The Experts below are selected from a list of 99 Experts worldwide ranked by ideXlab platform
Massimo Zerani - One of the best experts on this subject based on the ideXlab platform.
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role of nitric oxide in gonadotropin releasing hormone dependent prostaGlandin f2α synthesis by frog rana esculenta Interrenal Gland during post reproduction
Prostaglandins & Other Lipid Mediators, 1998Co-Authors: Anna Gobbetti, L Bellinicardellini, Massimo ZeraniAbstract:Abstract The aim of this study was to clarify the possible involvement of nitric oxide (NO) on prostaGlandin (PG) E2-9-ketoreductase activity in the gonadotropin-releasing hormone (GnRH)-dependent PGF2α synthesis by the Interrenal Gland of the female water frog, Rana esculenta, during the post-reproduction. Interrenal Glands were incubated in vitro with GnRH, NO donor (sodium nitroprusside, SNP), and inhibitors of phospholipase C (compound 48/80), inositol triphosphate (decavanadate), calmodulin (calmidazolium), NO synthase ( L -NAME), and PGE2-9-ketoreductase (palmitic acid). Production of PGE2 and PGF2α and NO synthase and PGE2-9-ketoreductase activities were determined. GnRH and SNP increased PGF2α production and PGE2-9-ketoreductase activity, and decreased production of PGE2 and GnRH increased NO synthase activity. GnRH effects were blocked by all inhibitors, except for palmitic acid, which did not affect NO synthase activity, which is increased by GnRH. This study indicates that NO may be involved in regulation of the R. esculenta post-reproduction through stimulation of PGE2-9-ketoreductase activity in GnRH-dependent PGF2α synthesis by the frog Interrenal Gland.
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gonadotropin releasing hormone stimulates biosynthesis of prostaGlandin f2α by the Interrenal Gland of the water frog rana esculenta in vitro
General and Comparative Endocrinology, 1991Co-Authors: Anna Gobbetti, Massimo ZeraniAbstract:Abstract The present study was carried out to evaluate the in vitro effects of mammalian gonadotropin-releasing hormone (mGnRH) on the production of prostaGlandin F2α(PGF2α) and sex steroids (progesterone, androgens, and 17β-estradiol) by the Interrenal Gland of male and female Rana esculenta during three different periods of the sexual annual cycle. In both sexes, mGnRH induced a significant increase in PGF2α in the incubation medium in all examined periods. Progesterone and androgens were undetectable, while 17β-estradiol was significantly increased by mGnRH in Interrenals incubated during the postreproductive period in both sexes. These results suggest that R. esculenta Interrenals could be a GnRH-dependent PGF2α-secreting tissue. In addition, the simultaneous increase in PGF2α and estradiol from postreproductive cultured Interrenals support the notion that mGnRH-induced estradiol synthesis is mediated through PGF2α formation. This finding, taken to-gether with other previous studies, strongly suggests that the end of the breeding period in R. esculenta depends on GnRH-induced PGF2α-mediated enhancement of estradiol synthesis in a steroidogenetic organ (probably Interrenals).
Anna Gobbetti - One of the best experts on this subject based on the ideXlab platform.
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role of nitric oxide in gonadotropin releasing hormone dependent prostaGlandin f2α synthesis by frog rana esculenta Interrenal Gland during post reproduction
Prostaglandins & Other Lipid Mediators, 1998Co-Authors: Anna Gobbetti, L Bellinicardellini, Massimo ZeraniAbstract:Abstract The aim of this study was to clarify the possible involvement of nitric oxide (NO) on prostaGlandin (PG) E2-9-ketoreductase activity in the gonadotropin-releasing hormone (GnRH)-dependent PGF2α synthesis by the Interrenal Gland of the female water frog, Rana esculenta, during the post-reproduction. Interrenal Glands were incubated in vitro with GnRH, NO donor (sodium nitroprusside, SNP), and inhibitors of phospholipase C (compound 48/80), inositol triphosphate (decavanadate), calmodulin (calmidazolium), NO synthase ( L -NAME), and PGE2-9-ketoreductase (palmitic acid). Production of PGE2 and PGF2α and NO synthase and PGE2-9-ketoreductase activities were determined. GnRH and SNP increased PGF2α production and PGE2-9-ketoreductase activity, and decreased production of PGE2 and GnRH increased NO synthase activity. GnRH effects were blocked by all inhibitors, except for palmitic acid, which did not affect NO synthase activity, which is increased by GnRH. This study indicates that NO may be involved in regulation of the R. esculenta post-reproduction through stimulation of PGE2-9-ketoreductase activity in GnRH-dependent PGF2α synthesis by the frog Interrenal Gland.
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gonadotropin releasing hormone stimulates biosynthesis of prostaGlandin f2α by the Interrenal Gland of the water frog rana esculenta in vitro
General and Comparative Endocrinology, 1991Co-Authors: Anna Gobbetti, Massimo ZeraniAbstract:Abstract The present study was carried out to evaluate the in vitro effects of mammalian gonadotropin-releasing hormone (mGnRH) on the production of prostaGlandin F2α(PGF2α) and sex steroids (progesterone, androgens, and 17β-estradiol) by the Interrenal Gland of male and female Rana esculenta during three different periods of the sexual annual cycle. In both sexes, mGnRH induced a significant increase in PGF2α in the incubation medium in all examined periods. Progesterone and androgens were undetectable, while 17β-estradiol was significantly increased by mGnRH in Interrenals incubated during the postreproductive period in both sexes. These results suggest that R. esculenta Interrenals could be a GnRH-dependent PGF2α-secreting tissue. In addition, the simultaneous increase in PGF2α and estradiol from postreproductive cultured Interrenals support the notion that mGnRH-induced estradiol synthesis is mediated through PGF2α formation. This finding, taken to-gether with other previous studies, strongly suggests that the end of the breeding period in R. esculenta depends on GnRH-induced PGF2α-mediated enhancement of estradiol synthesis in a steroidogenetic organ (probably Interrenals).
Yi-wen Liu - One of the best experts on this subject based on the ideXlab platform.
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The Hemodynamically-Regulated Vascular Microenvironment Promotes Migration of the Steroidogenic Tissue during Its Interaction with Chromaffin Cells
2016Co-Authors: In The Zebrafish Embryo, Chih-wei Chou, You-lin Zhuo, Zhe-yu Jiang, Yi-wen LiuAbstract:Background: While the endothelium-organ interaction is critical for regulating cellular behaviors during development and disease, the role of blood flow in these processes is only partially understood. The dorsal aorta performs paracrine functions for the timely migration and differentiation of the sympatho-adrenal system. However, it is unclear how the adrenal cortex and medulla achieve and maintain specific integration and whether hemodynamic forces play a role. Methodology and Principal Findings: In this study, the possible modulation of steroidogenic and chromaffin cell integration by blood flow was investigated in the teleostean counterpart of the adrenal Gland, the Interrenal Gland, in the zebrafish (Danio rerio). Steroidogenic tissue migration and angiogenesis were suppressed by genetic or pharmacologic inhibition of blood flow, and enhanced by acceleration of blood flow upon norepinephrine treatment. Repressed steroidogenic tissue migration and angiogenesis due to flow deficiency were recoverable following restoration of flow. The regulation of Interrenal morphogenesis by blood flow was found to be mediated through the vascular microenvironment and the Fibronectin-phosphorylated Focal Adhesion Kinase (Fn-pFak) signaling. Moreover, the knockdown of krüppel-like factor 2a (klf2a) or matrix metalloproteinase 2 (mmp2), two genes regulated by the hemodynamic force, phenocopied the defects in migration, angiogenesis, the vascular microenvironment, and pFak signaling of the steroidogenic tissue observed in flow-deficient embryos, indicating a direct requirement of mechanotransduction in these processes. Interestingly
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the hemodynamically regulated vascular microenvironment promotes migration of the steroidogenic tissue during its interaction with chromaffin cells in the zebrafish embryo
PLOS ONE, 2014Co-Authors: Chih-wei Chou, You-lin Zhuo, Zhe-yu Jiang, Yi-wen LiuAbstract:Background While the endothelium-organ interaction is critical for regulating cellular behaviors during development and disease, the role of blood flow in these processes is only partially understood. The dorsal aorta performs paracrine functions for the timely migration and differentiation of the sympatho-adrenal system. However, it is unclear how the adrenal cortex and medulla achieve and maintain specific integration and whether hemodynamic forces play a role. Methodology and Principal Findings In this study, the possible modulation of steroidogenic and chromaffin cell integration by blood flow was investigated in the teleostean counterpart of the adrenal Gland, the Interrenal Gland, in the zebrafish (Danio rerio). Steroidogenic tissue migration and angiogenesis were suppressed by genetic or pharmacologic inhibition of blood flow, and enhanced by acceleration of blood flow upon norepinephrine treatment. Repressed steroidogenic tissue migration and angiogenesis due to flow deficiency were recoverable following restoration of flow. The regulation of Interrenal morphogenesis by blood flow was found to be mediated through the vascular microenvironment and the Fibronectin-phosphorylated Focal Adhesion Kinase (Fn-pFak) signaling. Moreover, the knockdown of kruppel-like factor 2a (klf2a) or matrix metalloproteinase 2 (mmp2), two genes regulated by the hemodynamic force, phenocopied the defects in migration, angiogenesis, the vascular microenvironment, and pFak signaling of the steroidogenic tissue observed in flow-deficient embryos, indicating a direct requirement of mechanotransduction in these processes. Interestingly, epithelial-type steroidogenic cells assumed a mesenchymal-like character and downregulated β-Catenin at cell-cell junctions during interaction with chromaffin cells, which was reversed by inhibiting blood flow or Fn-pFak signaling. Blood flow obstruction also affected the migration of chromaffin cells, but not through mechanosensitive or Fn-pFak dependent mechanisms. Conclusions and Significance These results demonstrate that hemodynamically regulated Fn-pFak signaling promotes the migration of steroidogenic cells, ensuring their interaction with chromaffin cells along both sides of the midline during Interrenal Gland development.
Chih-wei Chou - One of the best experts on this subject based on the ideXlab platform.
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The Hemodynamically-Regulated Vascular Microenvironment Promotes Migration of the Steroidogenic Tissue during Its Interaction with Chromaffin Cells
2016Co-Authors: In The Zebrafish Embryo, Chih-wei Chou, You-lin Zhuo, Zhe-yu Jiang, Yi-wen LiuAbstract:Background: While the endothelium-organ interaction is critical for regulating cellular behaviors during development and disease, the role of blood flow in these processes is only partially understood. The dorsal aorta performs paracrine functions for the timely migration and differentiation of the sympatho-adrenal system. However, it is unclear how the adrenal cortex and medulla achieve and maintain specific integration and whether hemodynamic forces play a role. Methodology and Principal Findings: In this study, the possible modulation of steroidogenic and chromaffin cell integration by blood flow was investigated in the teleostean counterpart of the adrenal Gland, the Interrenal Gland, in the zebrafish (Danio rerio). Steroidogenic tissue migration and angiogenesis were suppressed by genetic or pharmacologic inhibition of blood flow, and enhanced by acceleration of blood flow upon norepinephrine treatment. Repressed steroidogenic tissue migration and angiogenesis due to flow deficiency were recoverable following restoration of flow. The regulation of Interrenal morphogenesis by blood flow was found to be mediated through the vascular microenvironment and the Fibronectin-phosphorylated Focal Adhesion Kinase (Fn-pFak) signaling. Moreover, the knockdown of krüppel-like factor 2a (klf2a) or matrix metalloproteinase 2 (mmp2), two genes regulated by the hemodynamic force, phenocopied the defects in migration, angiogenesis, the vascular microenvironment, and pFak signaling of the steroidogenic tissue observed in flow-deficient embryos, indicating a direct requirement of mechanotransduction in these processes. Interestingly
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the hemodynamically regulated vascular microenvironment promotes migration of the steroidogenic tissue during its interaction with chromaffin cells in the zebrafish embryo
PLOS ONE, 2014Co-Authors: Chih-wei Chou, You-lin Zhuo, Zhe-yu Jiang, Yi-wen LiuAbstract:Background While the endothelium-organ interaction is critical for regulating cellular behaviors during development and disease, the role of blood flow in these processes is only partially understood. The dorsal aorta performs paracrine functions for the timely migration and differentiation of the sympatho-adrenal system. However, it is unclear how the adrenal cortex and medulla achieve and maintain specific integration and whether hemodynamic forces play a role. Methodology and Principal Findings In this study, the possible modulation of steroidogenic and chromaffin cell integration by blood flow was investigated in the teleostean counterpart of the adrenal Gland, the Interrenal Gland, in the zebrafish (Danio rerio). Steroidogenic tissue migration and angiogenesis were suppressed by genetic or pharmacologic inhibition of blood flow, and enhanced by acceleration of blood flow upon norepinephrine treatment. Repressed steroidogenic tissue migration and angiogenesis due to flow deficiency were recoverable following restoration of flow. The regulation of Interrenal morphogenesis by blood flow was found to be mediated through the vascular microenvironment and the Fibronectin-phosphorylated Focal Adhesion Kinase (Fn-pFak) signaling. Moreover, the knockdown of kruppel-like factor 2a (klf2a) or matrix metalloproteinase 2 (mmp2), two genes regulated by the hemodynamic force, phenocopied the defects in migration, angiogenesis, the vascular microenvironment, and pFak signaling of the steroidogenic tissue observed in flow-deficient embryos, indicating a direct requirement of mechanotransduction in these processes. Interestingly, epithelial-type steroidogenic cells assumed a mesenchymal-like character and downregulated β-Catenin at cell-cell junctions during interaction with chromaffin cells, which was reversed by inhibiting blood flow or Fn-pFak signaling. Blood flow obstruction also affected the migration of chromaffin cells, but not through mechanosensitive or Fn-pFak dependent mechanisms. Conclusions and Significance These results demonstrate that hemodynamically regulated Fn-pFak signaling promotes the migration of steroidogenic cells, ensuring their interaction with chromaffin cells along both sides of the midline during Interrenal Gland development.
Scott B Nunez - One of the best experts on this subject based on the ideXlab platform.
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regulation of mrnas encoding the steroidogenic acute regulatory protein and cholesterol side chain cleavage enzyme in the elasmobranch Interrenal Gland
General and Comparative Endocrinology, 2010Co-Authors: Andrew N Evans, Scott B NunezAbstract:The rate-limiting and regulated step in steroidogenesis, the conversion of cholesterol to pregnenolone, is facilitated by the steroidogenic acute regulatory protein (StAR) and cytochrome P450 cholesterol side-chain cleavage (P450scc). We have isolated cDNAs encoding StAR and P450scc from the Atlantic stingray, Dasyatis sabina, and characterized the steroidogenic activity of the encoded proteins using a heterologous expression system. Green monkey kidney (COS-1) cells cotransfected with D. sabina StAR and human P450scc/adrenodoxin reductase/adrenodoxin fusion (F2) constructs produced significantly more pregnenolone than cells transfected with the F2 construct alone. COS-1 cells transfected with a modified F2 construct (F2DS) in which human P450scc is replaced by D. sabina P450scc had higher rates than cells transfected with D. sabina P450scc alone. In other vertebrates, the stress peptide adrenocorticotropic hormone (ACTH) elicits its effects on corticosteroidogenesis in part through regulation of StAR and P450scc mRNAs. In vitro incubation of D. sabina Interrenal tissue with porcine ACTH significantly increased intracellular cAMP and corticosteroid production. As demonstrated by quantitative PCR, ACTH also induced significant increases in mRNA abundance of both StAR and P450scc. Our results suggest that, as in higher vertebrates, chronic ACTH-induced glucocorticoid synthesis in elasmobranchs is mediated by regulation of primary steroidogenic mRNAs. This study is the first to demonstrate steroidogenic activity of an elasmobranch P450scc protein and express a composite elasmobranch steroidogenic pathway in a heterologous cell line. Also, the regulation of StAR and P450scc mRNAs has not previously been demonstrated in elasmobranch fishes.
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adaptation of a corticosterone elisa to demonstrate sequence specific effects of angiotensin ii peptides and c type natriuretic peptide on 1α hydroxycorticosterone synthesis and steroidogenic mrnas in the elasmobranch Interrenal Gland
The Journal of Steroid Biochemistry and Molecular Biology, 2010Co-Authors: Andrew N Evans, John M Rimoldi, Rama S V Gadepalli, Scott B NunezAbstract:It is thought that a single corticosteroid, 1α-hydroxycorticosterone (1α-B), is both a glucocorticoid and mineralocorticoid in the elasmobranch fishes. We investigated the putative mineralocorticoid role of 1α-B by examining regulation of Interrenal 1α-B synthesis by osmoregulatory hormones in the euryhaline stingray Dasyatis sabina. Using synthesized steroid, a commercial enzyme-linked immunoassay was validated for the quantification of 1α-B. In Interrenal cultures, the antinatriuretic peptide angiotensin II (ANG II) was potently steroidogenic, whereas C-type natriuretic peptide had no effect on 1α-B titers. However, both peptides significantly decreased abundance of rate-limiting steroidogenic mRNAs (steroidogenic acute regulatory protein, StAR; cholesterol side-chain cleavage, P450scc). We also isolated cDNAs encoding ANG II from three species of elasmobranch, verifying heterogeneity among elasmobranch peptides at the first amino acid position. Potential implications of this heterogeneity were investigated by examining the effects of homologous and heterologous ANG II on Interrenal steroid production and steroidogenic mRNAs. Changes at amino acid position three, but not position one, of ANG II significantly affected steroidogenic potency. Conversely, changes at position one, but not position three, significantly affected the potency of ANG II to alter levels of steroidogenic mRNAs. This study is the first to demonstrate regulation of elasmobranch steroidogenic mRNAs by osmoregulatory peptides.
