4.3 Article

The role of androgen in autophagy of granulosa cells from PCOS

期刊

GYNECOLOGICAL ENDOCRINOLOGY
卷 35, 期 8, 页码 669-672

出版社

TAYLOR & FRANCIS LTD
DOI: 10.1080/09513590.2018.1540567

关键词

Polycystic ovary syndrome; hyperandrogenism; autophagy; human granulosa cells; anovulation

资金

  1. National Natural Science Foundation of China [81571499, 81771648]
  2. Shanghai Municipal Education Commission-Gaofeng Clinical Medicine Grant Support [20161413]
  3. National Key R&D Program of China [2017YFC1001403]
  4. Program of Shanghai Academic Research Leader in Shanghai Municipal Commission of Health and Family Planning [2017BR015]
  5. Clinical Skills Improvement Project of Major Disorders, Hospital Development Center of Shanghai [16CR1022A]
  6. Shanghai Technological Innovation Plan [18140902400]

向作者/读者索取更多资源

Hyperandrogenism is one of the most common causes for anovulation in women and increases the risk for metabolic disorder in PCOS patients. Autophagy plays an important role in dysfunction of endocrine and anovulation. However, the relationship between hyperandrogenism and autophagy in human granulosa cells of PCOS patients remains unclear. By collecting granulosa cells from PCOS patients and non-PCOS patients, we found that the abundance of autophagy-related genes ATG5, ATG7, BECN1 mRNA and the ratio of autophagy marker protein light chain 3B II/I (LC3 II/I) were significantly increased whereas the abundance of the autophagy substrate SQSTM1/p62 was decreased in ovarian granulosa cells from PCOS patients. Furthermore, we demonstrated that BECN1 mRNA abundance in human granulosa cells positively correlated with the basal level of serum total testosterone and androgen up-regulated the abundance of BECN1 mRNA and the ratio of LC3II/LC3I in a dose-dependent manner in cultured granulosa cells. These observations indicated that androgen-induced activation of autophagy may play an important role in the development of PCOS and to explore the autophagy mechanisms involved in PCOS yield new insight into the pathophysiology and therapy of the disorder.

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