Inhibin

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Teresa K. Woodruff - One of the best experts on this subject based on the ideXlab platform.

  • Inhibin at 90 from discovery to clinical application a historical review
    Endocrine Reviews, 2014
    Co-Authors: Yogeshwar Makanji, Neena B. Schwartz, Jie Zhu, Rama K Mishra, Chris Holmquist, Winifred P Wong, Kelly E Mayo, Teresa K. Woodruff
    Abstract:

    When it was initially discovered in 1923, Inhibin was characterized as a hypophysiotropic hormone that acts on pituitary cells to regulate pituitary hormone secretion. Ninety years later, what we know about Inhibin stretches far beyond its well-established capacity to inhibit activin signaling and suppress pituitary FSH production. Inhibin is one of the major reproductive hormones involved in the regulation of folliculogenesis and steroidogenesis. Although the physiological role of Inhibin as an activin antagonist in other organ systems is not as well defined as it is in the pituitary-gonadal axis, Inhibin also modulates biological processes in other organs through paracrine, autocrine, and/or endocrine mechanisms. Inhibin and components of its signaling pathway are expressed in many organs. Diagnostically, Inhibin is used for prenatal screening of Down syndrome as part of the quadruple test and as a biochemical marker in the assessment of ovarian reserve. In this review, we provide a comprehensive summary of our current understanding of the biological role of Inhibin, its relationship with activin, its signaling mechanisms, and its potential value as a diagnostic marker for reproductive function and pregnancy-associated conditions.

  • an activin furin regulatory loop modulates the processing and secretion of Inhibin α and βb subunit dimers in pituitary gonadotrope cells
    Journal of Biological Chemistry, 2008
    Co-Authors: Monica Antenos, Niti M Jetly, Teresa K. Woodruff
    Abstract:

    Of all ligands of the transforming growth factor β superfamily, Inhibins and activins are a physiologically relevant pair that are functional antagonists of each other. Activin stimulates whereas Inhibin blocks follicle-stimulating hormone biosynthesis and secretion from pituitary gonadotrope cells, and together, Inhibin and activin control the pituitary gonadal axis essential for normal reproductive function. Sharing a similar β-subunit, the secretion of Inhibin heterodimers (α/β) or activin homodimers (β/β) as mature bioactive ligands depends, in part, on the proteolytic processing of precursor proteins. A short loop regulatory pathway controlling precursor processing and dimer secretion was discovered. Activin stimulates endogenous Inhibin α- and βB-subunit mRNA, protein, and proteolytic processing. Simultaneously, activin stimulated the proconvertase furin through a Smad2/3-dependent process. The data provide a mechanism where the regulation of furin and Inhibin subunits cooperates in an important positive short feedback loop. This regulatory loop augments the secretion of bioactive mature activin B, as well as Inhibin B dimers, necessary for local follicle-stimulating hormone β regulation.

  • Beta A versus beta B: is it merely a matter of expression?
    Molecular and Cellular Endocrinology, 2004
    Co-Authors: Thomas B. Thompson, Stacey C Chapman, Robert W. Cook, Theodore S. Jardetzky, Teresa K. Woodruff
    Abstract:

    Abstract Activins are members of the transforming growth factor (TGF) beta (β) superfamily of proteins that function in a wide array of physiological processes. Like other TGFβ ligands, activins are biologically active as dimers. An activin molecule is comprised of two β-subunits, of which four isoforms have been identified: βA, βB, βC, and βE. The most widely studied activins to date are activin A (βA/βA), activin B (βB/βB), and activin AB (βA/βB). Inhibin is a naturally occurring activin antagonist that consists of an α-subunit disulfide-linked to one of the activin β-subunits, producing Inhibin A (α/βA), or Inhibin B (α/βB). The development of assays distinguishing between different forms of activins and Inhibins, along with knock-in and knock-out models, have provided evidence that the βA- and βB-subunits have independent and separate roles physiologically. Additionally, evaluation of ligand–receptor interactions indicates significant differences in receptor affinity between activin isoforms, as well as between Inhibin isoforms. In this review we explore the differences between activin/Inhibin βA- and βB-subunits, including expression patterns, binding properties, and the specific structural aspects of each. From the growing pool of knowledge regarding activins and Inhibins, the emerging data support the hypothesis that βA- and βB-subunits are functionally differently.

  • Beta A versus beta B: is it merely a matter of expression?
    Molecular and cellular endocrinology, 2004
    Co-Authors: Thomas B. Thompson, Stacey C Chapman, Robert W. Cook, Theodore S. Jardetzky, Teresa K. Woodruff
    Abstract:

    Activins are members of the transforming growth factor (TGF) beta (beta) superfamily of proteins that function in a wide array of physiological processes. Like other TGFbeta ligands, activins are biologically active as dimers. An activin molecule is comprised of two beta-subunits, of which four isoforms have been identified: betaA, betaB, betaC, and betaE. The most widely studied activins to date are activin A (betaA/betaA), activin B (betaB/betaB), and activin AB (betaA/betaB). Inhibin is a naturally occurring activin antagonist that consists of an alpha-subunit disulfide-linked to one of the activin beta-subunits, producing Inhibin A (alpha/betaA), or Inhibin B (alpha/betaB). The development of assays distinguishing between different forms of activins and Inhibins, along with knock-in and knock-out models, have provided evidence that the betaA- and betaB-subunits have independent and separate roles physiologically. Additionally, evaluation of ligand-receptor interactions indicates significant differences in receptor affinity between activin isoforms, as well as between Inhibin isoforms. In this review we explore the differences between activin/Inhibin betaA- and betaB-subunits, including expression patterns, binding properties, and the specific structural aspects of each. From the growing pool of knowledge regarding activins and Inhibins, the emerging data support the hypothesis that betaA- and betaB-subunits are functionally differently.

  • Molecular biology of Inhibin action.
    Seminars in Reproductive Medicine, 2004
    Co-Authors: Robert W. Cook, Thomas B. Thompson, Theodore S. Jardetzky, Teresa K. Woodruff
    Abstract:

    Inhibins are dimeric glycoproteins that have primarily been studied for their role in antagonism of activin-mediated release of follicle-stimulating hormone (FSH) from gonadotropes of the anterior pituitary. As a member of the transforming growth factor beta (TGFbeta) superfamily of ligands and receptors, Inhibin shares several processing and structural features with other ligands of the family. An Inhibin molecule is composed of an alpha-subunit and a beta-subunit, and two isoforms have been widely investigated, Inhibin A (alpha/betaA) and Inhibin B (alpha/betaB). Each isoform undergoes processing from a large precursor protein to a mature 32- to 34-kDa form, depending upon the degree of glycosylation. In the absence of Inhibin, for example, in ovariectomized animals or postmenopausal women, serum FSH levels rise precipitously. In unilaterally ovariectomized animals the brief loss of Inhibin results in a sudden rise in FSH, which induces the remaining ovary to compensate with Inhibin subunit expression in a large number of antral follicles. FSH levels are restored and the cycle continues. These studies demonstrate the need for ovarian Inhibin to maintain normal gonadotropin levels. Recent studies have provided a mechanism of Inhibin action that is consistent with its role in reproduction and may expand Inhibin function to tissues outside the reproductive axis. Betaglycan is able to bind Inhibin, and in the presence of betaglycan, the affinity of Inhibin for activin receptors is increased 30-fold. Through interaction with the coreceptor, Inhibin can disrupt activin interaction with its receptors and can also disrupt the interaction of activin receptors with other members of the TGFbeta superfamily, such as the bone morphogenetic proteins. These new studies provide evidence for Inhibin activity in numerous organs throughout the body and for mediation of systems controlled by molecules other than activin.

Felice Petraglia - One of the best experts on this subject based on the ideXlab platform.

  • Inhibins in female and male reproductive physiology role in gametogenesis conception implantation and early pregnancy
    Human Reproduction Update, 2005
    Co-Authors: Stefano Luisi, Fernando M. Reis, Pasquale Florio, Felice Petraglia
    Abstract:

    A great deal of new information has arisen in the recent years concerning Inhibin physiology and clinical relevance in reproductive medicine. It is now recognized that the two Inhibin isoforms, named Inhibin A and Inhibin B, are produced by the gonads in the course of gamete maturation and in women have a different pattern of secretion throughout the menstrual cycle. Since Inhibins are also produced by placenta and fetal membranes, it has been suggested that there is an involvement in physiological adaptation of pregnancy. Evidence from several sources has underlined the clinical usefulness of the measurement of Inhibin-related proteins in the diagnosis and follow-up of different fertility disturbances and early pregnancy viability. In the male, Inhibin B is produced in the testis, principally by the Sertoli cells. Inhibin B expression and secretion are positively correlated with Sertoli cell function, sperm number, and spermatogenic status and are negatively correlated with FSH. This review covers the most recent advances on the role of Inhibins in human reproductive function. Considerable progress in the understanding of Inhibin physiology has resulted from selective measurement of the two Inhibin molecular forms, named Inhibin A and B. Newly recognized alterations of Inhibin levels in gynaecological diseases as well as in normal and pathological pregnancy are discussed, with particular emphasis on the potential clinical usefulness of assessing Inhibin levels in serum and other biological fluids.

  • Abnormal Umbilical Artery Doppler Waveforms and Cord Blood Inhibin A and Inhibin B Levels
    Neonatology, 2003
    Co-Authors: Pasquale Florio, Stefano Luisi, G. Calonaci, Filiberto Maria Severi, Erika Ignacchiti, Caterina Bocchi, Felice Petraglia
    Abstract:

    Inhibin A and Inhibin B are glycoprotein hormones produced by human placenta and by several fetal organs during pregnancy. They are secreted in maternal circulation in increasing amounts from early until term pregnancy, and in umbilical cord blood levels are significantly lower than in maternal serum and do not differ from mid-pregnancy to term gestation. In the present study, we aimed to determine whether secretion of Inhibin A and Inhibin B into the fetal circulation is increased in pregnancies complicated by umbilical-placental vascular insufficiency. A group of women (n = 13) with abnormal Doppler umbilical artery flow velocimetry and a group of control women (n = 11) with uncomplicated term pregnancies and normal umbilical artery flow velocity waveforms were studied. In each woman, Inhibin A and Inhibin B concentrations were estimated in umbilical cord artery and vein. In the two groups of women, mean Inhibin A levels did not differ between umbilical cord artery and vein. In addition, no difference was retrieved both in umbilical cord artery and vein values between healthy controls and patients with abnormal Doppler umbilical artery flow velocimetry. On the contrary, Inhibin B levels were significantly higher in samples from umbilical cord vein than artery, in both groups of pregnant women (both p < 0.001). However, women with abnormal Doppler umbilical artery flow velocimetry had Inhibin B levels significantly higher than healthy controls (p = 0.005) only in the umbilical cord artery, but not in the vein. In the presence of abnormal Doppler umbilical artery flow velocity, the concentrations of Inhibin B are increased in the arterial umbilical circulation, suggesting that Inhibin B is released from multiple fetal sources as a response to hypoxemic stress. As Inhibins may affect the hypothalamus-pituitary-adrenal axis which plays an important role in the mechanisms of adaptations to the post-natal life, Inhibin B in fetal circulation might then be beneficial to a fetus whose intrauterine survival is threatened by impaired umbilical-placental blood flow.

  • Inhibin A, Inhibin B and activin A concentrations in umbilical cord artery and vein.
    Gynecological Endocrinology, 2003
    Co-Authors: Pasquale Florio, Stefano Luisi, G. Calonaci, Filiberto Maria Severi, Erika Ignacchiti, M. Palumbo, Caterina Bocchi, Felice Petraglia
    Abstract:

    Activin A and Inhibins (A and B) are growth factors expressed during pregnancy by the human placenta ,decidua and fetal membranes ,and by several fetal organs. They are secreted in both the maternal and the fetal circulations ,but the net contribution of the fetus to Inhibins/activin A production is still unclear. In the present study we determined whether there was a difference in the serum concentration of activin A ,Inhibin A and Inhibin B between the artery and vein of the umbilical cord. Arterial and venous umbilical cord blood was obtained immediately before elective Cesarean section of 16 term infants from uncomplicated pregnancies. Inhibins and activin A levels were assayed by specific enzyme-linked immuno-sorbent assays. The paired t-test and linear regression analysis were used to calculate statistical significance. Inhibin A levels did not differ between the artery and vein of the umbilical cord. In contrast ,arterial Inhibin B levels were significantly (p < 0.001) lower ,and activin A concentr...

  • Inhibin A, Inhibin B and activin A concentrations in umbilical cord artery and vein
    Gynecological Endocrinology, 2003
    Co-Authors: P. Florio, Stefano Luisi, G. Calonaci, Filiberto Maria Severi, Erika Ignacchiti, M. Palumbo, Caterina Bocchi, Felice Petraglia
    Abstract:

    Activin A and Inhibins (A and B) are growth factors expressed during pregnancy by the human placenta, decidua and fetal membranes, and by several fetal organs. They are secreted in both the maternal and the fetal circulations, but the net contribution of the fetus to Inhibins/activin A production is still unclear. In the present study we determined whether there was a difference in the serum concentration of activin A, Inhibin A and Inhibin B between the artery and vein of the umbilical cord. Arterial and venous umbilical cord blood was obtained immediately before elective Cesarean section of 16 term infants from uncomplicated pregnancies. Inhibins and activin A levels were assayed by specific enzyme-linked immunosorbent assays. The paired t-test and linear regression analysis were used to calculate statistical significance. Inhibin A levels did not differ between the artery and vein of the umbilical cord. In contrast, arterial Inhibin B levels were significantly (p < 0.001) lower, and activin A concentrations significantly (p < 0.05) higher than the respective venous concentrations. A significant correlation between arterial and venous levels of Inhibin A (r = 0.591; p < 0.05), Inhibin B (r = 0.749; p < 0.0001) and activin A (r = 0.571; p < 0.05) was found. The present findings suggest that the human placenta is the main source of Inhibin B, and the fetus of activin A, in the umbilical cord. In light of the possible roles played by Inhibin and activin in erythroid differentiation, protection of neurons against brain injury and modulation of adrenal and pancreatic hormone release, the present data may be of help in evaluating their changes in the umbilical cord when gestational diseases occu

  • activin a Inhibin a Inhibin b and parturition changes of maternal and cord serum levels according to the mode of delivery
    British Journal of Obstetrics and Gynaecology, 1999
    Co-Authors: Pasquale Florio, M Santuz, Stefano Luisi, Alessandro David Genazzani, Chiara Benedetto, C Di Carlo, Luca Marozio, Felice Petraglia
    Abstract:

    Objective To evaluate whether activin A, Inhibin A, and Inhibin B levels in maternal and umbilical artery serum change according to the mode of delivery. Design Maternal and cord blood specimens were collected at term after spontaneous labour and vaginal delivery, or elective caesarean section. Setting Universities of Pisa, Turin, Naples and Udine. Population Forty–two healthy pregnant women, at 39–40 weeks of gestation, divided into two subgroups: group 1 vaginal delivery (n= 21), were delivered of 10 female and 11 male infants; group 2 elective caesarean section (n= 21), were delivered of 11 female and 10 male infants. Main outcome measures Serum activin A, Inhibin A, Inhibin B concentrations in maternal and umbilical cord blood. Results At vaginal delivery, maternal serum Inhibin A and Inhibin B levels were lower and activin A levels higher than at elective caesarean section. Maternal levels of activin A, Inhibin A and Inhibin B were constantly higher than in umbilical arterial blood, independent of the mode of delivery. No significant difference was observed in umbilical arterial serum levels of the three proteins between the two modes of delivery. Umbilical arterial serum activin A and Inhibin A concentrations did not show a significant difference between male and female infants in either vaginal or caesarean section, but male infants showed Inhibin B levels significantly higher than female, independent of the mode of delivery. Conclusions In the presence of active labour, the human placenta secretes larger amounts of activin A and lesser amounts of Inhibin A and Inhibin B into the maternal circulation. Inhibin–related proteins in the fetal circulation do not show differences according to the mode of delivery, suggesting that they have a different method of production or metabolic rate compared with maternal activin and Inhibins.

Wylie Vale - One of the best experts on this subject based on the ideXlab platform.

  • Inhibin: role and secretion in the rat.
    Recent Progress in Hormone Research, 2013
    Co-Authors: Catherine Rivier, Veronica J. Roberts, Helene Meunier, Wylie Vale
    Abstract:

    Publisher Summary This chapter discusses the role and secretion of Inhibin in the rat. The presently known mechanisms controlling luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion include gonadotropin-releasing hormone (GnRH), sex steroids, opiates, various neurotransmitters and peptides, Inhibin, activin, and follistatin. Inhibin—a molecule whose role was originally restricted to the specific inhibition of FSH secretion—is now recognized as an essential regulator of pituitary and gonadal function through complex effects of its own and interactions with other secretagogues, for example, activin, follistatin, Gn's, sex steroids, and GnRH. In the female endogenous, Inhibin appears to regulate both pituitary and gonadal activity. In the adult male (rat), the role of the protein might be restricted to testicular function. Despite numerous attempts toward purification and characterization of inhinbin, its structure has remained elusive. As a result of improvements in chromatography, protein sequence, and molecular cloning, a 32 kDa protein was isolated and characterized from ovine and bovine follicular fluids with the biological activities expected of Inhibin. Inhibin has an inhibitory action on fertility. The role of endogenous Inhibin in modulating FSH secretion in the male rat is restricted to the early part of sexual development. Immunoneutralization of endogenous Inhibin increases plasma FSH levels of young male rats, and this observation suggests a functional relationship between Inhibin and FSH secretion, which takes place until the relatively high plasma FSH levels characteristic of the adult male rat are established.

  • 4 Activins and Inhibins
    Cold Spring Harbor Monograph Archive, 2008
    Co-Authors: Ezra Wiater, Wylie Vale
    Abstract:

    Activins and the structurally and functionally related Inhibins belong to the transforming growth factor-β (TGF-β) family of growth factors. Activins and Inhibins have central roles in regulating follicle-stimulating hormone (FSH) release and in coordinating reproductive physiology. Inhibins function as classical endocrine hormones, whereas both activins and Inhibins have localized autocrine and paracrine roles. Activins have additional functions outside of the reproductive systems as regulators of cell growth and differentiation, particularly in response to injury and inflammation. This chapter discusses the mechanisms involved in activin and Inhibin activities and the roles of these factors in reproductive and other tissues. STRUCTURES AND SYNTHESIS OF ACTIVINS AND InhibinS A hormone termed “Inhibin” was proposed to exist in 1932 (McCullagh 1932). Inhibin was defined as a nonsteroidal, water-soluble factor in gonadal extracts that prevents stereotypical changes in the morphology of the pituitary that appeared after castration. After the identification of the pituitary cell types and their corresponding hormones, this definition was refined: Inhibin exerts a direct effect on pituitary gonadotrope cells, leading to a specific suppression of FSH release, without altering the release of luteinizing hormone (LH) (de Kretser et al. 1988; Vale et al. 1988). Biochemical purification of Inhibin was undertaken using this activity on pituitary cells as an assay. Secretions of various gonadal fluids were found to be rich sources of Inhibin and were thus used as source material for purification. Inhibins—and in the process, activins—were eventually purified to apparent homogeneity from these sources based on their effects on FSH...

  • identification of distinct Inhibin and transforming growth factor β binding sites on betaglycan functional separation of betaglycan co receptor actions
    Journal of Biological Chemistry, 2006
    Co-Authors: Ezra Wiater, Craig A. Harrison, Peter C. Gray, Kathy A Lewis, Wylie Vale
    Abstract:

    Betaglycan is a co-receptor that mediates signaling by transforming growth factor beta (TGFbeta) superfamily members, including the distinct and often opposed actions of TGFbetas and Inhibins. Loss of betaglycan expression, or abrogation of betaglycan function, is implicated in several human and animal diseases, although both betaglycan actions and the ligands involved in these disease states remain unclear. Here we identify a domain spanning amino acids 591-700 of the betaglycan extracellular domain as the only Inhibin-binding region in betaglycan. This binding site is within the betaglycan ZP domain, but Inhibin binding is not integral to the ZP motif of other proteins. We show that the Inhibin and TGFbeta-binding residues of this domain overlap and identify individual amino acids essential for binding of each ligand. Mutation of Val614 to Tyr abolishes both Inhibin and TGFbeta binding to this domain. Full-length betaglycan V614Y, and other mutations, retain TGFbeta binding activity via a distinct site, but are unable to bind Inhibin-A. These betaglycan mutants fail to mediate Inhibin antagonism of activin signaling but can present TGFbeta to TbetaRII. Separating the co-receptor actions of betaglycan toward Inhibin and TGFbeta will allow the clarification of the role of betaglycan in disease states such as renal cell carcinoma and endometrial adenocarcinoma.

  • Activins and Inhibins and Their Signaling
    Annals of the New York Academy of Sciences, 2004
    Co-Authors: Wylie Vale, Craig A. Harrison, Ezra Wiater, Peter C. Gray, Louise M. Bilezikjian, Senyon Choe
    Abstract:

    : Activins and Inhibins, which were discovered by virtue of their abilities to stimulate or inhibit, respectively, the secretion of FSH, are members of the transforming growth factor-beta (TGFbeta) superfamily and exert a broad range of effects on the diffentiation, proliferation and functions of numerous cell types. Activins interact with two structurally related classes of serine/threonine kinase receptors (type I and type II). Inhibin antagonizes activin by binding to the proteoglycan, betaglycan, and forming a stable complex with and, thereby, sequestering type II activin receptors while excluding type I receptors. If betaglycan is present, Inhibin can also antagonize those bone morphogenic proteins (BMPs) whose signaling is dependent upon access to type II activin receptors. Recent insights regarding the structures of ligands, receptors and their signaling complexes are providing the basis for the development of therapeutics capable of modulating fertility and numerous pathophysiologic processes.

  • Inhibin is an antagonist of bone morphogenetic protein signaling
    Journal of Biological Chemistry, 2003
    Co-Authors: Ezra Wiater, Wylie Vale
    Abstract:

    Abstract Inhibins are endogenous antagonists of activin signaling, long recognized as important regulators of gonadal function and pituitary FSH release. Inhibin, in concert with its co-receptor, betaglycan, can compete with activin for binding to type II activin receptors and, thus, prevent activin signaling. Because bone morphogenetic proteins (BMPs) also utilize type II activin receptors, we hypothesized that BMP signaling might also be sensitive to Inhibin blockade. Here we show that Inhibin blocks cellular responses to diverse BMP family members in a variety of BMP-responsive cell types. Inhibin abrogates BMP-induced Smad signaling and transcription responses. Inhibin competes with BMPs for type II activin receptors, and this competition is facilitated by betaglycan. Betaglycan also enables Inhibin to bind to and compete with BMPs for binding to the BMP-specific type II receptor BMPRII, which does not bind Inhibin in the absence of betaglycan. Betaglycan can confer Inhibin responsiveness on cells that are otherwise insensitive to Inhibin. These findings demonstrate that Inhibin, acting through betaglycan, can function as an antagonist of BMP responses, suggesting a broader role for Inhibin and betaglycan in restricting and refining a wide spectrum of transforming growth factor β superfamily signals.

Stefano Luisi - One of the best experts on this subject based on the ideXlab platform.

  • Inhibins in female and male reproductive physiology role in gametogenesis conception implantation and early pregnancy
    Human Reproduction Update, 2005
    Co-Authors: Stefano Luisi, Fernando M. Reis, Pasquale Florio, Felice Petraglia
    Abstract:

    A great deal of new information has arisen in the recent years concerning Inhibin physiology and clinical relevance in reproductive medicine. It is now recognized that the two Inhibin isoforms, named Inhibin A and Inhibin B, are produced by the gonads in the course of gamete maturation and in women have a different pattern of secretion throughout the menstrual cycle. Since Inhibins are also produced by placenta and fetal membranes, it has been suggested that there is an involvement in physiological adaptation of pregnancy. Evidence from several sources has underlined the clinical usefulness of the measurement of Inhibin-related proteins in the diagnosis and follow-up of different fertility disturbances and early pregnancy viability. In the male, Inhibin B is produced in the testis, principally by the Sertoli cells. Inhibin B expression and secretion are positively correlated with Sertoli cell function, sperm number, and spermatogenic status and are negatively correlated with FSH. This review covers the most recent advances on the role of Inhibins in human reproductive function. Considerable progress in the understanding of Inhibin physiology has resulted from selective measurement of the two Inhibin molecular forms, named Inhibin A and B. Newly recognized alterations of Inhibin levels in gynaecological diseases as well as in normal and pathological pregnancy are discussed, with particular emphasis on the potential clinical usefulness of assessing Inhibin levels in serum and other biological fluids.

  • Abnormal Umbilical Artery Doppler Waveforms and Cord Blood Inhibin A and Inhibin B Levels
    Neonatology, 2003
    Co-Authors: Pasquale Florio, Stefano Luisi, G. Calonaci, Filiberto Maria Severi, Erika Ignacchiti, Caterina Bocchi, Felice Petraglia
    Abstract:

    Inhibin A and Inhibin B are glycoprotein hormones produced by human placenta and by several fetal organs during pregnancy. They are secreted in maternal circulation in increasing amounts from early until term pregnancy, and in umbilical cord blood levels are significantly lower than in maternal serum and do not differ from mid-pregnancy to term gestation. In the present study, we aimed to determine whether secretion of Inhibin A and Inhibin B into the fetal circulation is increased in pregnancies complicated by umbilical-placental vascular insufficiency. A group of women (n = 13) with abnormal Doppler umbilical artery flow velocimetry and a group of control women (n = 11) with uncomplicated term pregnancies and normal umbilical artery flow velocity waveforms were studied. In each woman, Inhibin A and Inhibin B concentrations were estimated in umbilical cord artery and vein. In the two groups of women, mean Inhibin A levels did not differ between umbilical cord artery and vein. In addition, no difference was retrieved both in umbilical cord artery and vein values between healthy controls and patients with abnormal Doppler umbilical artery flow velocimetry. On the contrary, Inhibin B levels were significantly higher in samples from umbilical cord vein than artery, in both groups of pregnant women (both p < 0.001). However, women with abnormal Doppler umbilical artery flow velocimetry had Inhibin B levels significantly higher than healthy controls (p = 0.005) only in the umbilical cord artery, but not in the vein. In the presence of abnormal Doppler umbilical artery flow velocity, the concentrations of Inhibin B are increased in the arterial umbilical circulation, suggesting that Inhibin B is released from multiple fetal sources as a response to hypoxemic stress. As Inhibins may affect the hypothalamus-pituitary-adrenal axis which plays an important role in the mechanisms of adaptations to the post-natal life, Inhibin B in fetal circulation might then be beneficial to a fetus whose intrauterine survival is threatened by impaired umbilical-placental blood flow.

  • Inhibin A, Inhibin B and activin A concentrations in umbilical cord artery and vein.
    Gynecological Endocrinology, 2003
    Co-Authors: Pasquale Florio, Stefano Luisi, G. Calonaci, Filiberto Maria Severi, Erika Ignacchiti, M. Palumbo, Caterina Bocchi, Felice Petraglia
    Abstract:

    Activin A and Inhibins (A and B) are growth factors expressed during pregnancy by the human placenta ,decidua and fetal membranes ,and by several fetal organs. They are secreted in both the maternal and the fetal circulations ,but the net contribution of the fetus to Inhibins/activin A production is still unclear. In the present study we determined whether there was a difference in the serum concentration of activin A ,Inhibin A and Inhibin B between the artery and vein of the umbilical cord. Arterial and venous umbilical cord blood was obtained immediately before elective Cesarean section of 16 term infants from uncomplicated pregnancies. Inhibins and activin A levels were assayed by specific enzyme-linked immuno-sorbent assays. The paired t-test and linear regression analysis were used to calculate statistical significance. Inhibin A levels did not differ between the artery and vein of the umbilical cord. In contrast ,arterial Inhibin B levels were significantly (p < 0.001) lower ,and activin A concentr...

  • Inhibin A, Inhibin B and activin A concentrations in umbilical cord artery and vein
    Gynecological Endocrinology, 2003
    Co-Authors: P. Florio, Stefano Luisi, G. Calonaci, Filiberto Maria Severi, Erika Ignacchiti, M. Palumbo, Caterina Bocchi, Felice Petraglia
    Abstract:

    Activin A and Inhibins (A and B) are growth factors expressed during pregnancy by the human placenta, decidua and fetal membranes, and by several fetal organs. They are secreted in both the maternal and the fetal circulations, but the net contribution of the fetus to Inhibins/activin A production is still unclear. In the present study we determined whether there was a difference in the serum concentration of activin A, Inhibin A and Inhibin B between the artery and vein of the umbilical cord. Arterial and venous umbilical cord blood was obtained immediately before elective Cesarean section of 16 term infants from uncomplicated pregnancies. Inhibins and activin A levels were assayed by specific enzyme-linked immunosorbent assays. The paired t-test and linear regression analysis were used to calculate statistical significance. Inhibin A levels did not differ between the artery and vein of the umbilical cord. In contrast, arterial Inhibin B levels were significantly (p < 0.001) lower, and activin A concentrations significantly (p < 0.05) higher than the respective venous concentrations. A significant correlation between arterial and venous levels of Inhibin A (r = 0.591; p < 0.05), Inhibin B (r = 0.749; p < 0.0001) and activin A (r = 0.571; p < 0.05) was found. The present findings suggest that the human placenta is the main source of Inhibin B, and the fetus of activin A, in the umbilical cord. In light of the possible roles played by Inhibin and activin in erythroid differentiation, protection of neurons against brain injury and modulation of adrenal and pancreatic hormone release, the present data may be of help in evaluating their changes in the umbilical cord when gestational diseases occu

  • activin a Inhibin a Inhibin b and parturition changes of maternal and cord serum levels according to the mode of delivery
    British Journal of Obstetrics and Gynaecology, 1999
    Co-Authors: Pasquale Florio, M Santuz, Stefano Luisi, Alessandro David Genazzani, Chiara Benedetto, C Di Carlo, Luca Marozio, Felice Petraglia
    Abstract:

    Objective To evaluate whether activin A, Inhibin A, and Inhibin B levels in maternal and umbilical artery serum change according to the mode of delivery. Design Maternal and cord blood specimens were collected at term after spontaneous labour and vaginal delivery, or elective caesarean section. Setting Universities of Pisa, Turin, Naples and Udine. Population Forty–two healthy pregnant women, at 39–40 weeks of gestation, divided into two subgroups: group 1 vaginal delivery (n= 21), were delivered of 10 female and 11 male infants; group 2 elective caesarean section (n= 21), were delivered of 11 female and 10 male infants. Main outcome measures Serum activin A, Inhibin A, Inhibin B concentrations in maternal and umbilical cord blood. Results At vaginal delivery, maternal serum Inhibin A and Inhibin B levels were lower and activin A levels higher than at elective caesarean section. Maternal levels of activin A, Inhibin A and Inhibin B were constantly higher than in umbilical arterial blood, independent of the mode of delivery. No significant difference was observed in umbilical arterial serum levels of the three proteins between the two modes of delivery. Umbilical arterial serum activin A and Inhibin A concentrations did not show a significant difference between male and female infants in either vaginal or caesarean section, but male infants showed Inhibin B levels significantly higher than female, independent of the mode of delivery. Conclusions In the presence of active labour, the human placenta secretes larger amounts of activin A and lesser amounts of Inhibin A and Inhibin B into the maternal circulation. Inhibin–related proteins in the fetal circulation do not show differences according to the mode of delivery, suggesting that they have a different method of production or metabolic rate compared with maternal activin and Inhibins.

Pasquale Florio - One of the best experts on this subject based on the ideXlab platform.

  • Inhibins in female and male reproductive physiology role in gametogenesis conception implantation and early pregnancy
    Human Reproduction Update, 2005
    Co-Authors: Stefano Luisi, Fernando M. Reis, Pasquale Florio, Felice Petraglia
    Abstract:

    A great deal of new information has arisen in the recent years concerning Inhibin physiology and clinical relevance in reproductive medicine. It is now recognized that the two Inhibin isoforms, named Inhibin A and Inhibin B, are produced by the gonads in the course of gamete maturation and in women have a different pattern of secretion throughout the menstrual cycle. Since Inhibins are also produced by placenta and fetal membranes, it has been suggested that there is an involvement in physiological adaptation of pregnancy. Evidence from several sources has underlined the clinical usefulness of the measurement of Inhibin-related proteins in the diagnosis and follow-up of different fertility disturbances and early pregnancy viability. In the male, Inhibin B is produced in the testis, principally by the Sertoli cells. Inhibin B expression and secretion are positively correlated with Sertoli cell function, sperm number, and spermatogenic status and are negatively correlated with FSH. This review covers the most recent advances on the role of Inhibins in human reproductive function. Considerable progress in the understanding of Inhibin physiology has resulted from selective measurement of the two Inhibin molecular forms, named Inhibin A and B. Newly recognized alterations of Inhibin levels in gynaecological diseases as well as in normal and pathological pregnancy are discussed, with particular emphasis on the potential clinical usefulness of assessing Inhibin levels in serum and other biological fluids.

  • Abnormal Umbilical Artery Doppler Waveforms and Cord Blood Inhibin A and Inhibin B Levels
    Neonatology, 2003
    Co-Authors: Pasquale Florio, Stefano Luisi, G. Calonaci, Filiberto Maria Severi, Erika Ignacchiti, Caterina Bocchi, Felice Petraglia
    Abstract:

    Inhibin A and Inhibin B are glycoprotein hormones produced by human placenta and by several fetal organs during pregnancy. They are secreted in maternal circulation in increasing amounts from early until term pregnancy, and in umbilical cord blood levels are significantly lower than in maternal serum and do not differ from mid-pregnancy to term gestation. In the present study, we aimed to determine whether secretion of Inhibin A and Inhibin B into the fetal circulation is increased in pregnancies complicated by umbilical-placental vascular insufficiency. A group of women (n = 13) with abnormal Doppler umbilical artery flow velocimetry and a group of control women (n = 11) with uncomplicated term pregnancies and normal umbilical artery flow velocity waveforms were studied. In each woman, Inhibin A and Inhibin B concentrations were estimated in umbilical cord artery and vein. In the two groups of women, mean Inhibin A levels did not differ between umbilical cord artery and vein. In addition, no difference was retrieved both in umbilical cord artery and vein values between healthy controls and patients with abnormal Doppler umbilical artery flow velocimetry. On the contrary, Inhibin B levels were significantly higher in samples from umbilical cord vein than artery, in both groups of pregnant women (both p < 0.001). However, women with abnormal Doppler umbilical artery flow velocimetry had Inhibin B levels significantly higher than healthy controls (p = 0.005) only in the umbilical cord artery, but not in the vein. In the presence of abnormal Doppler umbilical artery flow velocity, the concentrations of Inhibin B are increased in the arterial umbilical circulation, suggesting that Inhibin B is released from multiple fetal sources as a response to hypoxemic stress. As Inhibins may affect the hypothalamus-pituitary-adrenal axis which plays an important role in the mechanisms of adaptations to the post-natal life, Inhibin B in fetal circulation might then be beneficial to a fetus whose intrauterine survival is threatened by impaired umbilical-placental blood flow.

  • Inhibin A, Inhibin B and activin A concentrations in umbilical cord artery and vein.
    Gynecological Endocrinology, 2003
    Co-Authors: Pasquale Florio, Stefano Luisi, G. Calonaci, Filiberto Maria Severi, Erika Ignacchiti, M. Palumbo, Caterina Bocchi, Felice Petraglia
    Abstract:

    Activin A and Inhibins (A and B) are growth factors expressed during pregnancy by the human placenta ,decidua and fetal membranes ,and by several fetal organs. They are secreted in both the maternal and the fetal circulations ,but the net contribution of the fetus to Inhibins/activin A production is still unclear. In the present study we determined whether there was a difference in the serum concentration of activin A ,Inhibin A and Inhibin B between the artery and vein of the umbilical cord. Arterial and venous umbilical cord blood was obtained immediately before elective Cesarean section of 16 term infants from uncomplicated pregnancies. Inhibins and activin A levels were assayed by specific enzyme-linked immuno-sorbent assays. The paired t-test and linear regression analysis were used to calculate statistical significance. Inhibin A levels did not differ between the artery and vein of the umbilical cord. In contrast ,arterial Inhibin B levels were significantly (p < 0.001) lower ,and activin A concentr...

  • activin a Inhibin a Inhibin b and parturition changes of maternal and cord serum levels according to the mode of delivery
    British Journal of Obstetrics and Gynaecology, 1999
    Co-Authors: Pasquale Florio, M Santuz, Stefano Luisi, Alessandro David Genazzani, Chiara Benedetto, C Di Carlo, Luca Marozio, Felice Petraglia
    Abstract:

    Objective To evaluate whether activin A, Inhibin A, and Inhibin B levels in maternal and umbilical artery serum change according to the mode of delivery. Design Maternal and cord blood specimens were collected at term after spontaneous labour and vaginal delivery, or elective caesarean section. Setting Universities of Pisa, Turin, Naples and Udine. Population Forty–two healthy pregnant women, at 39–40 weeks of gestation, divided into two subgroups: group 1 vaginal delivery (n= 21), were delivered of 10 female and 11 male infants; group 2 elective caesarean section (n= 21), were delivered of 11 female and 10 male infants. Main outcome measures Serum activin A, Inhibin A, Inhibin B concentrations in maternal and umbilical cord blood. Results At vaginal delivery, maternal serum Inhibin A and Inhibin B levels were lower and activin A levels higher than at elective caesarean section. Maternal levels of activin A, Inhibin A and Inhibin B were constantly higher than in umbilical arterial blood, independent of the mode of delivery. No significant difference was observed in umbilical arterial serum levels of the three proteins between the two modes of delivery. Umbilical arterial serum activin A and Inhibin A concentrations did not show a significant difference between male and female infants in either vaginal or caesarean section, but male infants showed Inhibin B levels significantly higher than female, independent of the mode of delivery. Conclusions In the presence of active labour, the human placenta secretes larger amounts of activin A and lesser amounts of Inhibin A and Inhibin B into the maternal circulation. Inhibin–related proteins in the fetal circulation do not show differences according to the mode of delivery, suggesting that they have a different method of production or metabolic rate compared with maternal activin and Inhibins.

  • low levels of serum Inhibin a and Inhibin b in women with hypergonadotropic amenorrhea and evidence of high levels of activin a in women with hypothalamic amenorrhea
    Fertility and Sterility, 1998
    Co-Authors: Felice Petraglia, Beda Hartmann, Silvia Kirchengast, M Santuz, Stefano Luisi, Pasquale Florio, Alessandro David Genazzani
    Abstract:

    Abstract Objective: To examine serum levels of Inhibin A, Inhibin B, and activin A in women with secondary hypergonadotropic or hypothalamic amenorrhea. Design: Retrospective study. Setting: Universities of Udine, Pisa, and Modena in Italy, and of Wien in Austria. Patient(s): Forty women with idiopathic premature ovarian failure (POF), 23 women with hypogonadotropic hypothalamic amenorrhea, 40 healthy postmenopausal women, and 40 age-matched women with normal ovarian function (controls). Intervention(s): Blood samples were collected between 8 and 9 am. Main Outcome Measure(s): Serum levels of Inhibin A, Inhibin B, and activin A. Result(s): Women with POF had lower concentrations of serum Inhibin A and Inhibin B than women with hypothalamic amenorrhea and fertile controls, and the difference between these concentrations was statistically significant. Levels of Inhibin A and Inhibin B were low in postmenopausal women and were no different than in women with POF. Serum levels of activin A were not significantly different among women with POF, fertile controls, and postmenopausal women. Women with hypogonadotropic hypothalamic amenorrhea had higher activin A values than did controls. No significant correlation was found between the level of Inhibin A or Inhibin B and the length of amenorrhea or the level of FSH. Conclusion(s): Low levels of circulating Inhibins A and B, but not activin A, reflect ovarian failure in women with POF, whereas women with hypogonadotropic hypothalamic amenorrhea have normal levels of Inhibins A and B and high levels of activin A.

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