RBM25 binds to and regulates alternative splicing levels of Slc38a9, Csf1, and Coro6 to affect immune and inflammatory processes in H9c2 cells

被引：2

作者：

Tian, Xin ^{[1
]}

Zhou, Guangli ^{[1
]}

Li, Hao ^{[1
]}

Zhang, Xueting ^{[1
]}

Zhao, Lingmin ^{[1
]}

Zhang, Keyi ^{[1
]}

Wang, Luqiao ^{[1
]}

Liu, Mingwei ^{[1
]}

Liu, Chen ^{[2
]}

Yang, Ping ^{[1
]}

机构：

[1] Kunming Med Univ, Affiliated Hosp 1, Dept Cardiol, Kunming, Peoples R China

[2] Yunnan Univ, Affiliated Hosp, Dept Radiol, Kunming, Peoples R China

来源：

PEERJ | 2023年 / 11卷

基金：

中国国家自然科学基金;

关键词：

RBM25; Alternative splicing; RNA-seq; Improved RNA immunoprecipitation sequencing; Inflammation; H9c2; cell; Heart failure; HEART-FAILURE; GENE-EXPRESSION; PROTEIN; IDENTIFICATION; HYPERTROPHY; MECHANISMS; APOPTOSIS;

D O I：

10.7717/peerj.16312

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Background. Alternative splicing (AS) is a biological process that allows genes to be translated into diverse proteins. However, aberrant AS can predispose cells to aberrations in biological mechanisms. RNA binding proteins (RBPs), closely affiliated with AS, have gained increased attention in recent years. Among these RBPs, RBM25 has been reported to participate in the cardiac pathological mechanism through regulating AS; however, the involvement of RBM25 as a splicing factor in heart failure remains unclarified. Methods. RBM25 was overexpressed in H9c2 cells to explore the target genes bound and regulated by RBM25 during heart failure. RNA sequencing (RNA-seq) was used to scrutinize the comprehensive transcriptional level before identifying AS events influenced by RBM25. Further, improved RNA immunoprecipitation sequencing (iRIP-seq) was employed to pinpoint RBM25-binding sites, and RT-qPCR was used to validate specific genes modulated by RBM25. Results. RBM25 was found to upregulate the expression of genes pertinent to the inflammatory response and viral processes, as well as to mediate the AS of genes associated with cellular apoptosis and inflammation. Overlap analysis between RNA-seq and iRIP-seq suggested that RBM25 bound to and manipulated the AS of genes associated with inflammation in H9c2 cells. Moreover, qRT-PCR confirmed Slc38a9, Csf1, and Coro6 as the binding and AS regulatory targets of RBM25. Conclusion. Our research implies that RBM25 plays a contributory role in cardiac inflammatory responses via its ability to bind to and regulate the AS of related genes. This study offers preliminary evidence of the influence of RBM25 on inflammation in H9c2 cells.

引用

页数：22