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Jing Xiong Institute of Pathology, Department of Pathophysiology, Tongji Hospital
Institute of Pathology, Department of Pathophysiology, Tongji Hospital

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Pan Zeng Institute of Pathology, Department of Pathophysiology, Tongji Hospital

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Xue Cheng Institute of Pathology, Department of Pathophysiology, Tongji Hospital

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Sen Miao Institute of Pathology, Department of Pathophysiology, Tongji Hospital

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Le Wu Institute of Pathology, Department of Pathophysiology, Tongji Hospital

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Sheng Zhou Institute of Pathology, Department of Pathophysiology, Tongji Hospital

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Ping Wu Institute of Pathology, Department of Pathophysiology, Tongji Hospital

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Duyun Ye Institute of Pathology, Department of Pathophysiology, Tongji Hospital

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Embryo implantation involves a complex regulatory network of steroid hormones, inflammatory cytokines, and immune cells. Lipoxin A4 (LXA4), a biologically active eicosanoid with specific anti-inflammatory and pro-resolving properties, was recently found to be a novel modulator of estrogen receptor α (ERα). In this study, we investigated the potential role of LXA4 in implantation. We found that LXA4 blocked embryo implantation in mice and significantly reduced the expression of inflammatory mediators associated with uterine receptivity and embryo implantation, including corticotropin-releasing factor (CRF), cyclooxygenase 2-derived prostaglandin I2 and prostaglandin E2, leukemia inhibitory factor, and interleukin 6, but this effect was independent of LXA4 receptor. Subsequent investigation revealed enhanced ERα activity in the uteri of LXA4-treated mice during the peri-implantation period. ERα and phosphorylated ERα were significantly increased following LXA4 treatment. Finally, it was demonstrated that the inhibitory effect of LXA4 on embryo implantation was mediated through ERα. In the presence of the ERα antagonist ICI 182 780, LXA4 failed to block embryo implantation. LXA4 also failed to inhibit CRF expression. These results suggested that LXA4 blocks embryo implantation by controlling ERα activity, and this effect appeared to be related to the suppression of the inflammatory microenvironment necessary for implantation.

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Canxin Wen Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China
State Key Laboratory of Reproductive Medicine and Offspring Health, Center for Reproductive Medicine, Institute of Women, Children and Reproductive Health,Shandong University, Jinan, Shandong, China
Guangdong Provincial Clinical Research Center for Obstetrical and Gynecological Diseases, Guangzhou, China

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Linlin Jiang Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China
Guangdong Provincial Clinical Research Center for Obstetrical and Gynecological Diseases, Guangzhou, China

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Ping Pan Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China
Guangdong Provincial Clinical Research Center for Obstetrical and Gynecological Diseases, Guangzhou, China

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Jia Huang Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China
Guangdong Provincial Clinical Research Center for Obstetrical and Gynecological Diseases, Guangzhou, China

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Yanxin Xie Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China
Guangdong Provincial Clinical Research Center for Obstetrical and Gynecological Diseases, Guangzhou, China

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Songbang Ou Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China
Guangdong Provincial Clinical Research Center for Obstetrical and Gynecological Diseases, Guangzhou, China

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Yu Li Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China
Guangdong Provincial Clinical Research Center for Obstetrical and Gynecological Diseases, Guangzhou, China

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In brief

Ovarian aging results in reactive oxygen species accumulation and mitochondrial deterioration. During the aging process, GRSF1 deficiency attenuates mitochondrial function in aging granulosa cells.

Abstract

Ovarian aging critically influences reproductive potential, with a marked decrease in oocyte quality and quantity and an increase in oxidative stress and mitochondrial dysfunction. This study elucidates the role of guanine-rich RNA sequence binding factor 1 (GRSF1) in the aging of ovarian granulosa cells (GCs). We observed a significant reduction in GRSF1 within GCs correlating with patient age, utilizing clinical samples from IVF patients. Using an siRNA-mediated knockdown technique, we established that diminished GRSF1 expression exacerbates mitochondrial dysfunction, elevates reactive oxygen species, and impairs ATP production. Furthermore, RNA immunoprecipitation revealed GRSF1’s interaction with superoxide dismutase 2 (SOD2) mRNA, a key antioxidant enzyme, suggesting a mechanism whereby GRSF1 modulates oxidative stress. Downregulation of SOD2 reversed the protective effects of GRSF1 overexpression on mitochondrial function. These insights into the role of GRSF1 in ovarian aging may guide the development of interventions to improve fertility outcomes in advanced age.

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