MAX deficiency impairs human endometrial decidualization through down-regulating OSR2 in women with recurrent spontaneous abortion

• DOI: 10.1007/s00441-022-03579-z
• Publication Date: 2022-02-11T04:29:58Z
• Authors: Weixu Ma; Mingzhu Cao; Shilei Bi; Lili Du; Jingsi Chen; Haibin Wang; Yufei Jiang; Yixuan Wu; Yixin Liao; Shuangbo Kong; Jianqiao Liu
• Keywords: Decidualization; Chromatin immunoprecipitation; Decidual cells; Decidua

Human uterine stromal cell undergoes decidualization for pregnancy establishment and maintenance, which involved extensive proliferation differentiation. Increasing studies have suggested that recurrent spontaneous abortion (RSA) may result from defective endometrial decidualization. However, the critical molecular mechanisms underlying impaired during RSA are still elusive. By using our recently published single-cell RNA sequencing (scRNA-seq) atlas, we found MYC-associated factor X (MAX) was significantly downregulated in cells derived decidual tissues of women with RSA, followed by verification immunohistochemistry (IHC) quantitative real-time polymerase chain reaction (qRT-PCR). MAX knockdown impairs human (HESCs) as determined MTS assay Ki67 immunostaining, F-actin, markers. RNA-seq together chromatin immunoprecipitation (ChIP-seq) cleavage under targets release nuclease (CUT&RUN-seq) analysis were applied to explore regulation decidualization, dual-luciferase reporter verify (odd-skipped related transcription 2) OSR2 directly. Reduced expression also confirmed IHC qRT-PCR. HESCs OSR2-overexpression could at least partly rescue insulin-like growth binding protein 1 (IGFBP1) level response knockdown. Collectively, deficiency observed not only attenuates but downregulating transcriptional