Academic Journal

miR-361-5p Mediates SMAD4 to Promote Porcine Granulosa Cell Apoptosis through VEGFA

التفاصيل البيبلوغرافية
العنوان: miR-361-5p Mediates SMAD4 to Promote Porcine Granulosa Cell Apoptosis through VEGFA
المؤلفون: Mengnan Ma, Jinbi Zhang, Xiaomeng Gao, Wang Yao, Qifa Li, Zengxiang Pan
المصدر: Biomolecules, Vol 10, Iss 9, p 1281 (2020)
بيانات النشر: MDPI AG, 2020.
سنة النشر: 2020
المجموعة: LCC:Microbiology
مصطلحات موضوعية: GC apoptosis, VEGFA, miR-361-5p, TGF-β signaling, SMAD4, follicular atresia, Microbiology, QR1-502
الوصف: Follicular atresia is an inevitable degenerative process that occurs in mammalian ovarian follicles. The molecular events involved in atresia, particularly granulosa cell apoptosis, have long attracted researchers’ attention. Vascular endothelial growth factor A (VEGFA) is downregulated during follicular atresia in porcine ovaries and serves as an inhibitor of apoptosis in granulosa cells. In addition, transforming growth factor (TGF)-βsignaling has been considered a central trigger in granulosa cell apoptosis. However, the link between TGF-β signaling and VEGFA is unknown. We proved that miR-361-5p is significantly upregulated during the atresia process and that it promotes GC apoptosis by directly targeting the VEGFA 3′UTR. In addition, we revealed that the miR-361-5p coding gene MIR361 was significantly downregulated by SMAD4, the central intracellular mediator of TGF-β signaling, that bound to the MIR361 promoter. In conclusion, our findings expanded what is known about VEGFA posttranscriptional regulation and revealed a complete SMAD4/miR-361-5p/VEGFA regulatory network in ovarian granulosa cell apoptosis. These data provide useful references for follicular atresia and ovarian physiological function studies.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2218-273X
Relation: https://www.mdpi.com/2218-273X/10/9/1281; https://doaj.org/toc/2218-273X
DOI: 10.3390/biom10091281
URL الوصول: https://doaj.org/article/4279b3b03f794b0d85801de5bf396c1c
رقم الانضمام: edsdoj.4279b3b03f794b0d85801de5bf396c1c
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:2218273X
DOI:10.3390/biom10091281