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TGF-β1 Down-Regulates Vascular Cell Adhesion Molecule 1 in Porcine Follicular Granulosa Cells Through Smad2
Yanzi Lin1, Haojie Ouyang1, Song Fu1
1Guangxi Key Laboratory of Animal Breeding and Disease Control, College of Animal Science and Technology, Guangxi University, Nanning, People's Republic of China.
The TGF-β/Smad signalling pathway plays a critical regulatory role in mammalian follicular development. Vascular Cell Adhesion Molecule 1 (VCAM1), as a member of the immunoglobulin (Ig) superfamily, is commonly expressed in various cells of the mammalian ovary and affects ovarian development. Previous studies have shown that TGF-β1 is a regulator that down-regulates the expression of VCAM1 in human granulosa cells, but its specific mechanism remains unclear. In this study, we revealed that in porcine follicular granulosa cells, TGF-β1 reduces VCAM1 expression by activating TGF-β receptor type I and through the Smad pathway. This down-regulation can be completely reversed by knockdown of Smad2, but not Smad3, suggesting that Smad2 may exert a non-redundant, specialised function in the regulation of VCAM1 by the TGF-β/Smad signalling pathway. These results enhance the understanding of the regulatory mechanisms of the TGF-β signalling pathway in reproduction and provide a theoretical basis for the regulation of reproductive traits.
The TGF-β/Smad signalling pathway plays a critical regulatory role in mammalian follicular development. Vascular Cell Adhesion Molecule 1 (VCAM1), as a member of the immunoglobulin (Ig) superfamily, is commonly expressed in various cells of the mammalian ovary and affects ovarian development. Previous studies have shown that TGF-β1 is a regulator that down-regulates the expression of VCAM1 in human granulosa cells, but its specific mechanism remains unclear. In this study, we revealed that in porcine follicular granulosa cells, TGF-β1 reduces VCAM1 expression by activating TGF-β receptor type I and through the Smad pathway. This down-regulation can be completely reversed by knockdown of Smad2, but not Smad3, suggesting that Smad2 may exert a non-redundant, specialised function in the regulation of VCAM1 by the TGF-β/Smad signalling pathway. These results enhance the understanding of the regulatory mechanisms of the TGF-β signalling pathway in reproduction and provide a theoretical basis for the regulation of reproductive traits.
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