دورية أكاديمية

Obesity-induced inflammatory miR-133a mediates apoptosis of granulosa cells and causes abnormal folliculogenesis

التفاصيل البيبلوغرافية
العنوان: Obesity-induced inflammatory miR-133a mediates apoptosis of granulosa cells and causes abnormal folliculogenesis
المؤلفون: Chen Ruizhi, Wu Xueqing, Qiu Han, Yang Baiming, Chen Yao, Chen Xiang, Li Yingshan, Yuan Shaochun, Liu Dan, Xiao Luanjuan, Yu Yanhong
المصدر: Acta Biochimica et Biophysica Sinica, Vol 55, Pp 1234-1246 (2023)
بيانات النشر: China Science Publishing & Media Ltd., 2023.
سنة النشر: 2023
المجموعة: LCC:Biochemistry
LCC:Genetics
مصطلحات موضوعية: abnormal follicular development, inflammation, miR-133a, obesity, Biochemistry, QD415-436, Genetics, QH426-470
الوصف: Obesity has been reported to promote disordered folliculogenesis, but the exact molecular mechanisms are still not fully understood. In this study, we find that miR-133a is involved in obesity-induced follicular development disorder. After feeding with a high-fat diet (HFD) and fructose water for nine weeks, the mouse body weight is significantly increased, accompanied by an inflammatory state and increased expression of miR-133a in the adipose tissues and ovaries as well as accelerated follicle depletion. Although miR-133a is increased in the fat and ovaries of HFD mice, the increased miR-133a in the HFD ovaries is not derived from exosome transferred from obese adipose tissues but is synthesized by ovarian follicular cells in response to HFD-induced inflammation. In vivo experiments show that intrabursal injection of miR-133a agomir induces a decrease in primordial follicles and an increase in antral follicles and atretic follicles, which is similar to HFD-induced abnormal folliculogenesis. Overexpression of miR-133a modestly promotes granulosa cell apoptosis by balancing the expression of anti-apoptotic proteins such as C1QL1 and XIAP and pro-apoptotic proteins such as PTEN. Overall, this study reveals the function of miR-133a in obesity-induced ovarian folliculogenesis dysfunction and sheds light on the etiology of female reproductive disorders.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1672-9145
العلاقة: https://doaj.org/toc/1672-9145Test
DOI: 10.3724/abbs.2023089
الوصول الحر: https://doaj.org/article/d8f821773a734a67af33fedcec284456Test
رقم الانضمام: edsdoj.8f821773a734a67af33fedcec284456
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:16729145
DOI:10.3724/abbs.2023089