Vui lòng dùng định danh này để trích dẫn hoặc liên kết đến tài liệu này: https://dspace.ctu.edu.vn/jspui/handle/123456789/71135
Nhan đề: miR-431 regulates granulosa cell function through the IRS2/PI3K/AKT signaling pathway
Tác giả: Yang, Lei
Lv, Qizhuang
Liu, Jianyun
Qi, Shikai
Fu, Denggang
Từ khoá: Cell proliferation
Estradiol
Granulosa cells
Insulin receptor substrate 2
miR-431
Năm xuất bản: 2020
Tùng thư/Số báo cáo: Journal of reproduction and development;Vol. 66, No. 03 .- P.231-239
Tóm tắt: MicroRNAs (miRNAs) regulate the functions of granulosa cells by interacting with their target mRNAs. Insulin receptor substrate 2 (IRS2) is one of the targets of miR-431 and can be regulated by ovarian hormones. However, the role of miR-431 and the associated signal transduction pathway in ovarian development has not been studied previously. In this study, we first analyzed the expression of miR-431 and IRS2 following stimulation with pregnant mare serum gonadotropin (PMSG) during the estrous cycle or different stages of ovarian development in mice. Subsequently, we investigated the role, function, and signaling pathway of miR-431 in the human granulosa cell line, COV434. The results showed that follicle stimulating hormone (FSH) gradually decreased miR-431 levels, induced IRS2, and promoted pAKT expression. Moreover, miR-431 overexpression and IRS2 knockdown attenuated AKT activation, inhibited cell proliferation, and decreased estradiol (E2) and progesterone ( P4) synthesis. Further, luciferase reporter assay demonstrated that IRS2 was a direct target of miR-431. In conclusion, this study demonstrated that miR-431 regulates granulosa cell function through the IRS2/PI3K/AKT signaling pathway.
Định danh: https://dspace.ctu.edu.vn/jspui/handle/123456789/71135
ISSN: 0916-8818
Bộ sưu tập: The journal of reproduction and development

Các tập tin trong tài liệu này:
Tập tin Mô tả Kích thước Định dạng  
_file_
  Giới hạn truy cập
2.89 MBAdobe PDF
Your IP: 18.223.108.134


Khi sử dụng các tài liệu trong Thư viện số phải tuân thủ Luật bản quyền.