Role of ALKBH5-mediated m6A modification in endometrial decidualization of mice in early pregnancy
10.13406/j.cnki.cyxb.003949
- VernacularTitle:ALKBH5介导的m6A修饰在早孕小鼠子宫内膜蜕膜化中的作用研究
- Author:
Sihui HE
1
;
Weike LI
;
Rufei GAO
;
Xuemei CHEN
;
Jing LONG
;
Chenxi CHEN
;
Dexian DAI
;
Yingxiong WANG
;
Na LI
Author Information
1. 重庆医科大学公共卫生学院生殖与发育教育部国际合作联合实验室,重庆 400016
- Keywords:
alkylation repair homolog 5;
N6-methyladenosine;
en-dometrial decidualization;
cell proliferation;
cell apoptosis
- From:
Journal of Chongqing Medical University
2025;50(11):1541-1549
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the role of alkylation repair homolog 5(ALKBH5)-mediated N6-methyladenosine(m6A)modifi-cation in endometrial decidualization.Methods:The mouse models of pregnancy and pseudopregnancy were established,and quantita-tive real-time PCR and Western blot were used to measure the expression pattern of ALKBH5 in the endometrium.The mouse and cell models of artificially induced decidualization were established,and quantitative real-time PCR,Western blot,and immunohistochemis-try were used to measure the expression levels of decidualization-related markers.The EpiQuik m6A RNA methylation quantification kit was used to measure the level of m6A.The mouse and cell models of artificially induced decidualization with interference of ALKBH5 expression were established,and quantitative real-time PCR,Western blot,and immunohistochemistry were used to measure the expression levels of decidualization-related markers,cell proliferation marker molecules,and apoptosis molecules.Flow cytometry was used to measure cell apoptosis rate.Results:In the mouse model of pregnancy,the expression level of ALKBH5 at the uterine em-bryo implantation site was significantly higher than that adjacent to the implantation site,and in the mouse and cell models of artifi-cially induced decidualization,compared with the control group,the induction group had a significant increase in the expression level of ALKBH5 and a significant reduction in the level of m6A.Inhibiting the expression of ALKBH5 led to an increase in the level of m6A,which in turn inhibited the proliferation of stromal cells,induced cell apoptosis,and ultimately impaired the normal process of en-dometrial decidualization.Conclusion:ALKBH5 deficiency leads to an increase in the level of m6A and decidualization injury in the en-dometrium,which lays a foundation for the research on m6A modifi-cation in decidualization.
