期刊
REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY
卷 20, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s12958-021-00881-3
关键词
Adenomyosis; Gonadotropin-releasing hormone agonist; Chemokine ligand 21; Endometrial receptivity
资金
- National Natural Science Foundation of China [81801530, 82071646]
This study identified differentially expressed genes (DEGs) in the endometrium of patients with adenomyosis after GnRHa treatment, indicating significant changes in immune system-associated signal transduction. The highly expressed chemokine (C-C motif) ligand 21 (CCL21) in the eutopic endometrium after GnRHa treatment may be involved in improving endometrial receptivity in adenomyosis.
Background Adenomyosis is a chronic gynecological disease characterized by invasion of the uterine endometrium into the muscle layer. In assisted reproductive technology (ART), gonadotropin-releasing hormone agonist (GnRHa) is often used to improve pregnancy rates in patients with adenomyosis, but the underlying mechanisms are poorly understood. Methods Eutopic endometrial specimens were collected from patients with adenomyosis before and after GnRHa treatment in the midsecretory phase. RNA sequencing (RNA-Seq) of these specimens was performed for transcriptome analysis. The differentially expressed genes (DEGs) of interest were confirmed by real-time PCR and immunohistochemistry. Results A total of 132 DEGs were identified in the endometrium of patients with adenomyosis after GnRHa treatment compared with the control group. Bioinformatics analysis predicted that immune system-associated signal transduction changed significantly after GnRHa treatment. Chemokine (C-C motif) ligand 21 (CCL21) was found to be highly expressed in the eutopic endometrium after GnRHa treatment, which may be involved in the improvement of endometrial receptivity in adenomyosis. Conclusion This study suggests that molecular regulation related to immune system-associated signal transduction is an important mechanism of GnRHa treatment in adenomyosis. Immunoreactive CCL21 is thought to regulate inflammatory events and participate in endometrial receptivity in adenomyosis.
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