PATL2 regulated the apoptosis of ovarian granulosa cells in patients with PCOS

Gynecol Endocrinol. 2021 Jul;37(7):629-634. doi: 10.1080/09513590.2021.1928066. Epub 2021 May 19.

Abstract

Aim: PCOS often showed abnormal follicular development. Previous studies have found that the increased apoptosis of granulosa cells (GCs) is one of the key factors leading to follicular dysplasia. It has been found that the decrease or deletion of PATL2 function can significantly inhibit the development and maturation of human oocytes. We found that PATL2 was also expressed in human ovarian GCs, suggesting that PATL2 may be involved in the regulation of related biological events in GCs. This study aims to explore the function of PATL2 on regulation of GCs apoptosis, and the potential role of PATL2 in the development of PCOS-related abnormal follicles.

Materials and methods: The follicular GCs of PCOS patients and normal ovulating female patients were collected. Moreover, human granular cell line (KGN) was used for in vitro experiments.

Results: (1) The maturation rate and fertilization rate of oocytes in the PCOS group were significantly lower than those in the normal control group (p<0.05). (2) Flow cytometry and TUNEL staining showed that the apoptosis level of GCs in the PCOS group was significantly increased. (3) Immunofluorescence and Western Blot showed that the PATL2 expression level of GCs in the PCOS group was significantly reduced. (4) Knocking down the expression of PATL2 by siRNA significantly prevented the apoptosis of GCs.

Conclusions: Reduced PATL2 could resulted in the increased apoptosis level of ovarian GCs, which might be closely related to the occurrence and development of abnormal follicles in PCOS.

Keywords: GCs; PATL2; PCOS; apoptosis.

MeSH terms

  • Adult
  • Apoptosis / genetics*
  • Blotting, Western
  • Case-Control Studies
  • Female
  • Fertilization in Vitro
  • Flow Cytometry
  • Gene Knockdown Techniques
  • Granulosa Cells / metabolism*
  • Humans
  • In Situ Nick-End Labeling
  • Nuclear Proteins / genetics*
  • Ovarian Follicle / abnormalities
  • Ovarian Follicle / metabolism*
  • Polycystic Ovary Syndrome / genetics*
  • RNA-Binding Proteins / genetics*

Substances

  • Nuclear Proteins
  • PATL2 protein, human
  • RNA-Binding Proteins