RhoA/ROCK/ARHGAP26 signaling in the eutopic and ectopic endometrium is involved in clinical characteristics of adenomyosis

Author:

Jiang Caixia1,Gong Wei2,Chen Rong1,Ke Huihui2,Qu Xiaoyan1,Yang Weihong1,Cheng Zhongping3

Affiliation:

1. Department of Gynecology and Obstetrics, Yangpu Hospital, Tongji University School of Medicine, Shanghai, China

2. Department of Gynecology and Obstetrics, Shanghai Pudong Hospital, Fudan University School of Medicine, Shanghai, China

3. Department of Gynecology and Obstetrics, Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, China

Abstract

Objective This study aimed to investigate RhoA, RhoA-associated coiled-coil containing protein kinase (ROCK) 1, ROCK2, and Rho GTPase-activating protein 26 (ARHGAP26) expression in the eutopic endometrium (EU) and ectopic endometrium (EC), and examine their relationships with the clinical characteristics of adenomyosis. Methods Twenty patients with adenomyosis who underwent laparoscopy were recruited. Protein and mRNA expression of RhoA, ROCK1, ROCK2, and ARHGAP26 in EU and EC of patients with adenomyosis and in control endometrium without adenomyosis (CE) was detected. Results ROCK1, ROCK2, and RhoA mRNA expression in EU was significantly higher than that in CE, and was highest in EC. ARHGAP26 mRNA expression in EC and EU was significantly lower than that in CE. ROCK1, ROCK2, and RhoA protein expression in EC and EU was significantly higher than that in CE. ARHGAP26 protein expression in EC and EU was significantly lower than that in CE. ROCK1, ROCK2, and RhoA gene and protein expression was positively associated and ARHGAP26 was negatively associated with the severity of menorrhagia and menstrual capacity in adenomyosis. Conclusions RhoA, ROCK1, and ROCK2 expression is upregulated, and ARHGAP26 expression is downregulated in adenomyosis. The RhoA/ROCK-mediated signaling pathway is associated with dysmenorrhea and menstrual capacity in adenomyosis.

Funder

Shanghai Municipal Health and Family Planning Commission

Publisher

SAGE Publications

Subject

Biochemistry (medical),Cell Biology,Biochemistry,General Medicine

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