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Abstract <p>Glutamine (Gln) has been shown to alleviate renal ischemia-reperfusion injury (IRI), but the underlying post-transcriptional regulatory mechanisms remain unclear. In this study, we performed transcriptomic analysis of neutrophils from a mouse IRI model (GSE188628) with or without Gln treatment to explore the role of RNA-binding proteins (RBPs) and alternative splicing (AS). We identified 47 differentially expressed RBP genes (DERBPs) significantly associated with transcriptional regulation, immune system development, and apoptosis-related pathways. Among them, Surf2 and Cpsf2 were significantly downregulated following Gln treatment and were highly correlated with altered splicing patterns in transcription factors, which regulated downstream genes involved in neutrophil apoptosis, a key process in IRI pathology. Experimental validation in a IRI mouse model confirmed that Gln administration significantly reduced cell apoptosis, serum injury biomarkers, as well as Surf2 and Cpsf2 expression. In conclusion, our study reveals a previously unrecognized RBP–AS–TF regulatory axis underlying the protective effects of Gln in renal IRI, offering new insight into neutrophil-regulated apoptosis and providing novel molecular targets for therapeutic intervention.</p>

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Genome-Wide Identification of Alternative Splicing and RNA-Binding Proteins Regulators Respond to Glutamine Therapy for Acute Kidney Injury

  • 期刊论文

  • 发表日期：

    2026年7月9日

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  • Sh. Wang,
  • H. Chen,
  • W. Maierziya,
  • Sh. Wang,
  • S. Ba,
  • Y. Li,
  • L. Zhang,
  • G. Zhu,
  • C. Lu

摘要

Abstract

Glutamine (Gln) has been shown to alleviate renal ischemia-reperfusion injury (IRI), but the underlying post-transcriptional regulatory mechanisms remain unclear. In this study, we performed transcriptomic analysis of neutrophils from a mouse IRI model (GSE188628) with or without Gln treatment to explore the role of RNA-binding proteins (RBPs) and alternative splicing (AS). We identified 47 differentially expressed RBP genes (DERBPs) significantly associated with transcriptional regulation, immune system development, and apoptosis-related pathways. Among them, Surf2 and Cpsf2 were significantly downregulated following Gln treatment and were highly correlated with altered splicing patterns in transcription factors, which regulated downstream genes involved in neutrophil apoptosis, a key process in IRI pathology. Experimental validation in a IRI mouse model confirmed that Gln administration significantly reduced cell apoptosis, serum injury biomarkers, as well as Surf2 and Cpsf2 expression. In conclusion, our study reveals a previously unrecognized RBP–AS–TF regulatory axis underlying the protective effects of Gln in renal IRI, offering new insight into neutrophil-regulated apoptosis and providing novel molecular targets for therapeutic intervention.