S100A11 promotes lipid metabolism and activates the apoptosis in polycystic ovary syndrome

in Reproduction
Authors:
Xiao Yang X Yang, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, China, Shandong University, Jinan, China

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Qi Jiang Q Jiang, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, China, Shandong University, Jinan, China

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Yanbo Du Y Du, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, China, Shandong University, Jinan, China

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Lei Yan L Yan, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, China, Shandong University, Jinan, China

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Hong Lv H Lv, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, China, Shandong University, Jinan, China

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Muzi Li M Li, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, China, Shandong University, Jinan, China

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Zihan Xu Z Xu, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, China, Shandong University, Jinan, China

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Correspondence: Lei Yan, Email: yanlei@sdu.edu.cn
DOI:
https://doi.org/10.1530/REP-24-0232
Volume/Issue:
Accepted Manuscripts
Article ID:
REP-24-0232
Article Type:
Research Article
Online Publication Date:
01 Dec 2024
Copyright:
© 2024 Society for Reproduction and Fertility 2024
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Apoptosis of ovarian granulosa cells (GCs) affects the development and maturation of oocyte in Polycystic ovary syndrome (PCOS).The objective of our study was to examine the impact of S100A11 on granulosa cells in individuals with polycystic ovary syndrome. We found that the S100A11 level was higher in the ovarian granulosa cells of PCOS patients and ovarian tissue of PCOS mouse models. S100A11 overexpression experiments demonstrated a decrease in the cell proliferation, upregulating the apoptosis and blocking the cell cycle. Immunofluorescence staining showed that S100A11 proteins were mainly located in the nucleus. Integrating the RNA-seq and ChIP-seq, this study found that S100A11 mainly regulated the genetic transcription and lipid metabolism. Furthermore, lipid accumulation and oxidative stress increasing were detected in the S100A11 overexpression group. We also revealed that S100A11 upregulated the p-DRP1 Ser616 to induce the mitochondrial fission.In conclusion, S100A11 upregulated the phospho-DRP1 to activate ovarian granulosa cell apoptosis and induced the lipid metabolism and oxidative stress to regulate the follicular reserve in PCOS. The findings present a novel therapeutic concept for polycystic ovary syndrome.

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Print ISSN:
1470-1626
Online ISSN:
1741-7899