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Regulation and Function of Laminin A5 during Mouse and Human Decidualization
Authors:Zhen-Shan Yang  Hai-Yang Pan  Wen-Wen Shi  Si-Ting Chen  Ying Wang  Meng-Yuan Li  Hai-Yi Zhang  Chen Yang  Ai-Xia Liu  Zeng-Ming Yang
Affiliation:1.College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China; (Z.-S.Y.); (H.-Y.P.); (W.-W.S.); (S.-T.C.); (Y.W.); (M.-Y.L.); (H.-Y.Z.); (C.Y.);2.Department of Reproductive Endocrinology, Women’s Hospital, School of Medicine, Zhejiang University, Xueshi Road, Hangzhou 310006, China
Abstract:Decidualization is essential to the establishment of pregnancy in rodents and primates. Laminin A5 (encoding by Laminin α5) is a member of the laminin family, which is mainly expressed in the basement membranes. Although laminins regulate cellular phenotype maintenance, adhesion, migration, growth, and differentiation, the expression, function, and regulation of laminin A5 during early pregnancy are still unknown. Therefore, we investigated the expression and role of laminin A5 during mouse and human decidualization. Laminin A5 is highly expressed in mouse decidua and artificially induced deciduoma. Laminin A5 is significantly increased under in vitro decidualization. Laminin A5 knockdown significantly inhibits the expression of Prl8a2, a marker for mouse decidualization. Progesterone stimulates the expression of laminin A5 in ovariectomized mouse uterus and cultured mouse stromal cells. We also show that progesterone regulates laminin A5 through the PKA-CREB-C/EBPβ pathway. Laminin A5 is also highly expressed in human pregnant decidua and cultured human endometrial stromal cells during in vitro decidualization. Laminin A5 knockdown by siRNA inhibits human in vitro decidualization. Collectively, our study reveals that laminin A5 may play a pivotal role during mouse and human decidualization via the PKA-CREB-C/EBPβ pathway.
Keywords:decidualization  laminin A5  uterus  PKA  CREB  C/EBPβ  
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