OGN inhibits apoptosis and ferroptosis via FSHR in human granulosa cells: implications for polycystic ovary syndrome.

Authors

Yu Zhang, Cheng Yin, Jiahui Wang, Jiajia Chen, Cuiping Li, Lijing Liu, Shi Liu

Published in

Cytotechnology. Volume 78. Issue 4. Pages 154. Epub Jul 10, 2026.

Abstract

Background Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by granulosa cell dysfunction, including impaired proliferation, excessive apoptosis, and ferroptosis, which contribute to abnormal follicular development and ovarian dysfunction. This study aims to investigate the effects of Osteoglycin (OGN) on proliferation, apoptosis, and ferroptosis in human ovarian granulosa cells, and to analyze its regulation of follicle stimulating hormone receptor (FSHR), providing insights into granulosa cell dysfunction associated with PCOS. Methods This study investigated the function of OGN in KGN granulosa cells by transfecting them with OGN-plasmid for overexpression or OGN-siRNA for knockdown. Cell viability was assessed using the MTT assay, while apoptosis was analyzed by flow cytometry. Ferroptosis was evaluated by measuring intracellular ROS and MDA levels, and protein expression was examined via Western blotting. Additionally, RT-qPCR and Western blotting were used to assess mRNA and protein levels of FSHR to determine the regulatory effect of OGN on FSHR expression. Results Overexpression of OGN significantly promoted granulosa cell proliferation and inhibited apoptosis, whereas knockdown of OGN suppressed proliferation and induced apoptosis. Mechanistic studies revealed that knockdown of OGN upregulated cleaved-Caspase3 expression, increased intracellular ROS and MDA levels, and reduced GPX4 expression, indicating the activation of both apoptotic and ferroptotic pathways. Furthermore, OGN positively regulated FSHR expression, as FSHR levels were increased with OGN overexpression and decreased following OGN knockdown at both mRNA and protein levels. Conclusion This study demonstrates that OGN plays a critical role in regulating granulosa cell survival and ferroptosis and may contribute to follicular development and PCOS-related ovarian dysfunction by modulating FSHR.

PMID:
42437191
Bibliographic data and abstract were imported from PubMed on 12 Jul 2026.

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