Role of SAA1 in Endometrial Extracellular Matrix Remodeling in Polycystic Ovary Syndrome: Implication for Pregnancy Loss

Qinling Zhu, Yuan Wang, Lizhen Xu, Mengjia Shi, Yiwen Meng, Congwen Shao, Chongwen Shao, Yao Lu, Yaqiong He, Jiaan Huang, Xinyu Li, Boyu Li, Yijing Long, Ying Ding, Jia Qi, Wangsheng Wang, Yanzhi Du, Yun Sun
In: The Journal of Clinical Endocrinology & Metabolism · 2024 · vol. 110(3) , pp. 658–667 · doi:10.1210/clinem/dgae596 · PMID:39210610 · W4402103437
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Elevated SAA1 in PCOS endometrium stimulates collagen I synthesis, promoting extracellular matrix overdeposition and increasing pregnancy loss risk.

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Abstract

CONTEXT: Abnormal endometrial extracellular matrix (ECM) remodeling compromises endometrial receptivity and diminishes the probability of a successful live birth. Serum amyloid A1 (SAA1), a modulator of inflammation, is elevated in the circulation of polycystic ovary syndrome (PCOS) patients and involved in ECM remodeling during tissue repair. However, the specific role of SAA1 in endometrial ECM remodeling and subsequent risk of pregnancy loss in PCOS patients remains unclear. OBJECTIVE: To examine the role and underlying mechanism of SAA1 in ECM remodeling in the endometrium of PCOS patients. DESIGN: Serum samples from PCOS and control patients were utilized to investigate the relationship between the abundance of SAA1 and pregnancy loss. Human endometrial tissues and primary human endometrial stromal cells were used to examine the role and underlying mechanism of SAA1 in ECM remodeling. RESULTS: Serum SAA1 concentration was elevated and could serve as an independent risk of pregnancy loss in PCOS patients. Increased SAA1 abundance was also observed in endometrium obtained from these patients. Further mechanistic studies showed that SAA1 stimulated collagen I chains synthesis (COL1A1 and COL1A2) in endometrial stromal cells, suggesting excessive SAA1 may contribute to endometrial ECM remodeling, resulting in a nonsupportive environment for ongoing pregnancy. This effect was abolished by either a toll-like receptor 2/4 antagonist or a nuclear factor κB inhibitor. CONCLUSION: The locally elevated levels of SAA1 in endometrium contribute to ECM overdeposition by inducing collagen I synthesis in PCOS patients, which may hamper embryo implantation and increase the risk of pregnancy loss. These observations highlight the crucial role of heightened SAA1 in orchestrating endometrial dysfunction and shed light on potential therapeutic avenues for improving reproductive outcomes in PCOS patients.

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