TGFβ1 Activates Opposing Effects through Different R-Smads in Enhancing FSH-Induced Steroidogenesis in Rat Granulosa Cells

碩士 === 國立陽明大學 === 生理學研究所 === 94 === Follicle-stimulating hormone (FSH), a pituitary hormone critically regulates ovarian folliculogenesis, stimulates granulosa cell proliferation and differentiation, and these actions are enhanced by ovarian factor transforming growth factor β (TGFβ). Till now, litt...

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Main Authors: HSIANG-TING HUANG, 黃湘婷
Other Authors: Jiuan-Jiuan Hwang
Format: Others
Language:en_US
Published: 2006
Online Access:http://ndltd.ncl.edu.tw/handle/97520260244105197324
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spelling ndltd-TW-094YM0051160082015-10-13T16:31:16Z http://ndltd.ncl.edu.tw/handle/97520260244105197324 TGFβ1 Activates Opposing Effects through Different R-Smads in Enhancing FSH-Induced Steroidogenesis in Rat Granulosa Cells 乙型轉型生長因子活化不同的R-Smads分子影響卵泡促素所誘導大鼠顆粒細胞類固醇生合成之效應 HSIANG-TING HUANG 黃湘婷 碩士 國立陽明大學 生理學研究所 94 Follicle-stimulating hormone (FSH), a pituitary hormone critically regulates ovarian folliculogenesis, stimulates granulosa cell proliferation and differentiation, and these actions are enhanced by ovarian factor transforming growth factor β (TGFβ). Till now, little is known regarding the molecular mechanism(s) whereby TGFβ synergizes FSH action to induce granulosa cell differentiation. The canonical and best characterized signaling pathway of TGFβ is mediated by ALK5/Smad2/3. Currently, an alternative lateral signaling pathway of TGFβ is through ALK1/Smad1 pathway and NFκB. Therefore, the objective of the present study was to investigate the participation of these two pathways in TGFβ1 enhancement on FSH-induced steroidogenesis in rat granulosa cells. TGFβ1 plus FSH dramatically induced the phosphorylation activation of Smad2 and Smad3 within 0.5 h to 1 h, and activating state declined to basal levels at 24 h and 48 h. Interestingly, TGFβ1 plus FSH increased Smad2/3 phosphorylation with greater potency than TGFβ1 alone. Also, a specific inhibitor of TβRI, SB431542 blocked TGFβ1-induced activation of Smad2 and 3, and this is consistent to our previous observation in TGFβ1 enhancement of FSH-induced steroidogenesis. Additionally, a specific NFκB inhibitor, SN50 dose-dependently elevated the FSH plus TGFβ1-stimulated progesterone production, and increased P450scc enzyme level. Together, this study demonstrates for the first time that FSH enhances the TGFβ1 signaling through TβRI-induced phosphorylation activation of Smad2 and 3 in rat ovarian granulosa cells. And NFκB activation opposes the Smad2/3 positive regulation of FSH plus TGFβ1-induced steroidogenesis in rat granulosa cells. Jiuan-Jiuan Hwang 黃娟娟 2006 學位論文 ; thesis 70 en_US
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language en_US
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description 碩士 === 國立陽明大學 === 生理學研究所 === 94 === Follicle-stimulating hormone (FSH), a pituitary hormone critically regulates ovarian folliculogenesis, stimulates granulosa cell proliferation and differentiation, and these actions are enhanced by ovarian factor transforming growth factor β (TGFβ). Till now, little is known regarding the molecular mechanism(s) whereby TGFβ synergizes FSH action to induce granulosa cell differentiation. The canonical and best characterized signaling pathway of TGFβ is mediated by ALK5/Smad2/3. Currently, an alternative lateral signaling pathway of TGFβ is through ALK1/Smad1 pathway and NFκB. Therefore, the objective of the present study was to investigate the participation of these two pathways in TGFβ1 enhancement on FSH-induced steroidogenesis in rat granulosa cells. TGFβ1 plus FSH dramatically induced the phosphorylation activation of Smad2 and Smad3 within 0.5 h to 1 h, and activating state declined to basal levels at 24 h and 48 h. Interestingly, TGFβ1 plus FSH increased Smad2/3 phosphorylation with greater potency than TGFβ1 alone. Also, a specific inhibitor of TβRI, SB431542 blocked TGFβ1-induced activation of Smad2 and 3, and this is consistent to our previous observation in TGFβ1 enhancement of FSH-induced steroidogenesis. Additionally, a specific NFκB inhibitor, SN50 dose-dependently elevated the FSH plus TGFβ1-stimulated progesterone production, and increased P450scc enzyme level. Together, this study demonstrates for the first time that FSH enhances the TGFβ1 signaling through TβRI-induced phosphorylation activation of Smad2 and 3 in rat ovarian granulosa cells. And NFκB activation opposes the Smad2/3 positive regulation of FSH plus TGFβ1-induced steroidogenesis in rat granulosa cells.
author2 Jiuan-Jiuan Hwang
author_facet Jiuan-Jiuan Hwang
HSIANG-TING HUANG
黃湘婷
author HSIANG-TING HUANG
黃湘婷
spellingShingle HSIANG-TING HUANG
黃湘婷
TGFβ1 Activates Opposing Effects through Different R-Smads in Enhancing FSH-Induced Steroidogenesis in Rat Granulosa Cells
author_sort HSIANG-TING HUANG
title TGFβ1 Activates Opposing Effects through Different R-Smads in Enhancing FSH-Induced Steroidogenesis in Rat Granulosa Cells
title_short TGFβ1 Activates Opposing Effects through Different R-Smads in Enhancing FSH-Induced Steroidogenesis in Rat Granulosa Cells
title_full TGFβ1 Activates Opposing Effects through Different R-Smads in Enhancing FSH-Induced Steroidogenesis in Rat Granulosa Cells
title_fullStr TGFβ1 Activates Opposing Effects through Different R-Smads in Enhancing FSH-Induced Steroidogenesis in Rat Granulosa Cells
title_full_unstemmed TGFβ1 Activates Opposing Effects through Different R-Smads in Enhancing FSH-Induced Steroidogenesis in Rat Granulosa Cells
title_sort tgfβ1 activates opposing effects through different r-smads in enhancing fsh-induced steroidogenesis in rat granulosa cells
publishDate 2006
url http://ndltd.ncl.edu.tw/handle/97520260244105197324
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