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Activin and Inhibin

The Experts below are selected from a list of 228 Experts worldwide ranked by ideXlab platform

Dana Gaddy – 1st expert on this subject based on the ideXlab platform

  • regulation of osteoblastogenesis and osteoclastogenesis by the other reproductive hormones Activin and Inhibin
    Molecular and Cellular Endocrinology, 2009
    Co-Authors: Kristy M Nicks, Daniel S Perrien, Nisreen S Akel, Larry J Suva, Dana Gaddy

    Abstract:

    There is both cellular and physiological evidence demonstrating that both Activins and Inhibins regulate osteoblastogenesis and osteoclastogenesis, and regulate bone mass in vivo. Although Activins and Inhibins were initially isolated from the gonad, Activins are also produced and stored in bone, whereas Inhibins exert their regulation on bone cell differentiation and metabolism via endocrine effects. The accumulating data provide evidence that reproductive hormones, distinct from classical sex steroids, are important regulators of bone mass and bone strength. Given the well described dominant antagonism of Inhibin over Activin, as well as over BMPs and TGFβ, the gonadally derived Inhibins are important regulators of locally produced osteotrophic factors. Thus, the cycling Inhibins in females and diurnal changes in Inhibin B in males elicit temporal shifts in Inhibin levels (tone) that de-repress the pituitary. This fundamental action has the potential to de-repress locally stimulated changes in osteoblastogenesis and osteoclastogenesis, thereby altering bone metabolism.

  • Regulation of osteoblastogenesis and osteoclastogenesis by the other reproductive hormones, Activin and Inhibin.
    Molecular and cellular endocrinology, 2009
    Co-Authors: Kristy M Nicks, Daniel S Perrien, Nisreen S Akel, Larry J Suva, Dana Gaddy

    Abstract:

    There is both cellular and physiological evidence demonstrating that both Activins and Inhibins regulate osteoblastogenesis and osteoclastogenesis, and regulate bone mass in vivo. Although Activins and Inhibins were initially isolated from the gonad, Activins are also produced and stored in bone, whereas Inhibins exert their regulation on bone cell differentiation and metabolism via endocrine effects. The accumulating data provide evidence that reproductive hormones, distinct from classical sex steroids, are important regulators of bone mass and bone strength. Given the well described dominant antagonism of Inhibin over Activin, as well as over BMPs and TGFbeta, the gonadally derived Inhibins are important regulators of locally produced osteotrophic factors. Thus, the cycling Inhibins in females and diurnal changes in Inhibin B in males elicit temporal shifts in Inhibin levels (tone) that de-repress the pituitary. This fundamental action has the potential to de-repress locally stimulated changes in osteoblastogenesis and osteoclastogenesis, thereby altering bone metabolism.

Jennie P. Mather – 2nd expert on this subject based on the ideXlab platform

  • localization of Inhibin and Activin binding sites in the testis during development by in situ ligand binding
    Biology of Reproduction, 1994
    Co-Authors: Lynne A. Krummen, Teresa K. Woodruff, Alison Moore, Robin Covello, Robin Taylor, Jennie P. Mather

    Abstract:

    : Inhibin and Activin are related proteins thought to be potential paracrine regulators of testicular development and maintenance of spermatogenesis. Messenger RNA and proteins immunologically related to both factors have been identified in the adult testis. However, the role(s) of these factors in paracrine regulation of testicular function is poorly understood. To identify potential targets for Inhibin and Activin in immature and adult testis, we used in situ binding of [125I]-labeled ligands to localize and describe the distribution of binding sites for Inhibin and Activin in testes of 15-, 18-, 21-, 30-, 45-, and 60-day-old rats. Nonspecific binding was defined as that occurring in the presence of a 1000-fold excess of unlabeled recombinant human (rh) Inhibin or Activin. [125I]-Inhibin was found to bind to interstitial cells throughout development. Inhibin binding was shown to co-localize with cells that showed positive staining for 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD). Competition studies demonstrated that this binding was indeed specific for Inhibin. In contrast, [125I]-Activin showed two distinct patterns of binding. First, [125I]-Activin was shown to bind in a non-stage-dependent manner to cells located in the basal compartment of the seminiferous tubules in testis obtained from animals of all ages studied. Binding of [125I]-Activin in the periphery of the tubule could be inhibited entirely by coincubation with excess unlabeled Activin and partially with excess unlabeled Inhibin. The ability of Inhibin to compete with Activin for binding appeared to be more pronounced in younger animals. In 45- and 60-day-old animals, a second stage-dependent component of [125I]-Activin binding was also apparent. This binding was localized to spermatids found in stage VII-VIII tubules and was inhibited by the presence of excess Activin, but not Inhibin. These results indicate that Inhibin can bind specifically to testicular interstitial cells throughout development and may be an important regulator of Leydig cell testosterone production or interstitial cell function. In contrast, Activin appears to bind in a specific and stage-dependent manner to receptors or high-affinity binding proteins on spermatids as well as to sites on the periphery of all seminiferous tubules. These results support the hypothesis that both Activin and Inhibin may act at several levels to regulate proliferation or differentiation of germ and Sertoli cell function as well as to modulate interstitial cell activity.

  • Inhibins, Activins, their binding proteins and receptors: interactions underlying paracrine activity in the testis.
    Molecular and Cellular Endocrinology, 1994
    Co-Authors: Alison Moore, Lynne A. Krummen, Jennie P. Mather

    Abstract:

    Abstract The Inhibin-related peptides are present in the testis from early gestation through adulthood. They are produced from multiple testicular sites in a highly regulated manner, suggesting important paracrine roles. Similarly, receptors for these peptides are located in specific stages of the seminiferous tubule and on particular cell types, and an additional level of control is afforded by specific binding proteins, such as follistatin, which may regulate bioavailability. The actions of these factors include the modulation of interstitial cell function and the increase of spermatogonial proliferation in vitro. It thus appears that Activin and Inhibin are significant factors in the local control of testicular funtion.

  • identification and characterization of binding proteins for Inhibin and Activin in human serum and follicular fluids
    Endocrinology, 1993
    Co-Authors: Lynne A. Krummen, Teresa K. Woodruff, Geralyn E Deguzman, Deborah L Baly, Elizabeth Mann, S Garg, Wai Lee Wong, Paul Cossum, Jennie P. Mather

    Abstract:

    Inhibins and Activins are produced by a variety of tissues and may have important endocrine and paracrine roles in development, reproduction, and hematopoiesis. However, little is known regarding the physical properties or concentrations of Inhibin and Activin in biological fluids. Binding proteins for Inhibin or Activin in serum or at production or target sites may have important implications for restricting the bioactivity of these hormones and may alter the immunoreactivity of these molecules in biological fluids. The objective of this study was to identify Inhibinand Activin-binding proteins in human serum (HS) and follicular fluid (hFF) and determine the ability of these proteins to alter biological or immunological activity. In HS, [125I]Activin and Inhibin bound to a protein identified as alpha 2-macroglobulin (alpha 2M) using three criteria: 1) [125I]Inhibin and Activin bind purified alpha 2M, but not several other serum proteins tested; 2) complexes formed by [125I]Inhibin and Activin in HS and

Daniel S Perrien – 3rd expert on this subject based on the ideXlab platform

  • regulation of osteoblastogenesis and osteoclastogenesis by the other reproductive hormones Activin and Inhibin
    Molecular and Cellular Endocrinology, 2009
    Co-Authors: Kristy M Nicks, Daniel S Perrien, Nisreen S Akel, Larry J Suva, Dana Gaddy

    Abstract:

    There is both cellular and physiological evidence demonstrating that both Activins and Inhibins regulate osteoblastogenesis and osteoclastogenesis, and regulate bone mass in vivo. Although Activins and Inhibins were initially isolated from the gonad, Activins are also produced and stored in bone, whereas Inhibins exert their regulation on bone cell differentiation and metabolism via endocrine effects. The accumulating data provide evidence that reproductive hormones, distinct from classical sex steroids, are important regulators of bone mass and bone strength. Given the well described dominant antagonism of Inhibin over Activin, as well as over BMPs and TGFβ, the gonadally derived Inhibins are important regulators of locally produced osteotrophic factors. Thus, the cycling Inhibins in females and diurnal changes in Inhibin B in males elicit temporal shifts in Inhibin levels (tone) that de-repress the pituitary. This fundamental action has the potential to de-repress locally stimulated changes in osteoblastogenesis and osteoclastogenesis, thereby altering bone metabolism.

  • Regulation of osteoblastogenesis and osteoclastogenesis by the other reproductive hormones, Activin and Inhibin.
    Molecular and cellular endocrinology, 2009
    Co-Authors: Kristy M Nicks, Daniel S Perrien, Nisreen S Akel, Larry J Suva, Dana Gaddy

    Abstract:

    There is both cellular and physiological evidence demonstrating that both Activins and Inhibins regulate osteoblastogenesis and osteoclastogenesis, and regulate bone mass in vivo. Although Activins and Inhibins were initially isolated from the gonad, Activins are also produced and stored in bone, whereas Inhibins exert their regulation on bone cell differentiation and metabolism via endocrine effects. The accumulating data provide evidence that reproductive hormones, distinct from classical sex steroids, are important regulators of bone mass and bone strength. Given the well described dominant antagonism of Inhibin over Activin, as well as over BMPs and TGFbeta, the gonadally derived Inhibins are important regulators of locally produced osteotrophic factors. Thus, the cycling Inhibins in females and diurnal changes in Inhibin B in males elicit temporal shifts in Inhibin levels (tone) that de-repress the pituitary. This fundamental action has the potential to de-repress locally stimulated changes in osteoblastogenesis and osteoclastogenesis, thereby altering bone metabolism.