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Updated: Aug 13, 2026
A Modified Technique for Inducing Polycystic Ovary Syndrome in Mice
Published on: July 5, 2024
Integrated Transcriptomic and DNA Methylation Analysis Reveals ITGB2-Mediated Immune Dysregulation in Polycystic
Peng Yi1, Ying Cao2, Yanru Zhou2
1Center of Reproductive Medicine, Quzhou People's Hospital, The Quzhou Affiliated Hospital, Wenzhou Medical University, Quzhou, Zhejiang, 324000, China. yipengqz@wmu.edu.cn.
Objectives:
To identify immune-related molecular targets in polycystic ovary syndrome (PCOS) and evaluate the role of integrin beta-2 (ITGB2) and the potential modulation by rutin.
Methods:
Follicular fluid cytokines from 30 women with PCOS and 30 control women were profiled. Transcriptomic (GSE34526) and DNA methylation (GSE138573) data were integrated to identify overlapping genes, followed by functional enrichment analyses, protein-protein interaction (PPI), and molecular docking analyses. LPS-stimulated granulosa cells, in the presence or absence of ITGB2 overexpression and rutin treatment, were assessed for gene expression, viability, cytokine secretion, and NF-κB activation.
Results:
Women with PCOS had higher IL-5 but lower IL-1β and IL-12p70. ITGB2, ITGAM, and CD86 were upregulated and hypomethylated. Among these, ITGB2 bound rutin with the lowest energy (- 7.8 kcal/mol). Rutin reduced ITGB2 expression, restored viability, suppressed cytokine release, and inhibited NF-κB activation, even under ITGB2 overexpression.
Conclusion:
ITGB2 is associated with inflammatory responses in granulosa cells and may contribute to PCOS-related immune dysregulation via NF-κB activation. Rutin attenuates these inflammatory responses, supporting a potential involvement of the ITGB2/NF-κB axis as a therapeutic target.
Clinical Trial Number:
Not applicable.
