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Transforming growth factor-beta 1 disrupts angiogenesis during the follicular-luteal transition through the Smad-serpin family E member 1 (SERPINE1)/serpin family B member 5 (SERPINB5) signalling pathway in the cow

文献类型： 外文期刊

作者： Yan, Leyan 1 ; Qu, Xiaolu 1 ; Yu, Jianning 1 ; Robinson, Robert S. 3 ; Woad, Kathryn J. 3 ; Shi, Zhendan 1 ;

作者机构： 1.Jiangsu Acad Agr Sci, Inst Anim Sci, Lab Anim Improvement & Reprod, Nanjing 210014, Peoples R China

2.Jiangsu Acad Agr Sci, State Key Lab Cultivat Base, Jiangsu Key Lab Food Qual & Safety, Minist Sci & Technol, Nanjing 210014, Peoples R China

3.Univ Nottingham, Sch Vet Med & Sci, Sutton Bonington Campus, Loughborough LE12 5RD, Leics, England

关键词： angiogenesis; luteinisation; serpin family B member 5 (SERPINB5); serpin family E member 1 (SERPINE1); Smad; transforming growth factor-beta 1 (TGFB1)

期刊名称：REPRODUCTION FERTILITY AND DEVELOPMENT （ 影响因子：1.718； 五年影响因子：1.923 ）

ISSN： 1031-3613

年卷期：

页码：

收录情况： SCI

摘要： Intense angiogenesis is critical for the development of the corpus luteum and is tightly regulated by numerous factors. However, the exact role transforming growth factor-beta 1 (TGFB1) plays during this follicular-luteal transition remains unclear. This study hypothesised that TGFB1, acting through TGFB receptor 1 (TGFBR1) and Smad2/3 signalling, would suppress angiogenesis during the follicular-luteal transition. Using a serum-free luteinising follicular angiogenesis culture system, TGFB1 (1 and 10 ngmL(-1)) markedly disrupted the formation of capillary-like structures, reducing the endothelial cell network area and the number of branch points (P<0.001 compared with control). Furthermore, TGFB1 activated canonical Smad signalling and inhibited endothelial nitric oxide synthase (NOS3) mRNA expression, but upregulated latent TGFB-binding protein and TGFBR1, serpin family E member 1 (SERPINE1) and serpin family B member 5 (SERPINB5) mRNA expression. SB431542, a TGFBR1 inhibitor, reversed the TGFB1-induced upregulation of SERPINE1 and SERPINB5. In addition, TGFB1 reduced progesterone synthesis by decreasing the expression of steroidogenic acute regulatory protein (STAR), cytochrome P450 family 11 subfamily A member 1 (CYP11A1) and 3b-hydroxysteroid dehydrogenase (HSD3B1) expression. These results show that TGFB1 regulates NOS3, SERPINE1 and SERPINB5 expression via TGFBR1 and Smad2/3 signalling and this could be the mechanism by which TGFB1 suppresses endothelial networks. Thereby, TGFB1 may provide critical homeostatic control of angiogenesis during the follicular-luteal transition. The findings of this study reveal the molecular mechanisms underlying the actions of TGFB1 in early luteinisation, which may lead to novel therapeutic strategies to reverse luteal inadequacy.

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