Scholarlink

<p>ICH, a severe stroke, causes neuronal death, neuroinflammation, and cerebral edema due to mitochondrial and immune dysfunction. The molecular mechanisms of secondary brain injuries are unclear, limiting effective therapies. This study used bioinformatics and experiments to explore miR-940’s role in ICH. MitoDEGs were identified via MitoCarta 3.0, and key miRNAs predicted using TargetScan and miRDB. A collagenase-induced ICH rat model with antagomir knockdown was used for validation. Neuronal damage, mitochondrial proteins, and immune cell dynamics were assessed using histopathology, qRT-PCR, Western blotting, and flow cytometry. Bioinformatics identified seven MitoDEGs and miR-940. Functional analysis linked them to mitochondrial metabolism and neuroinflammation. Inhibiting miR-940 in vivo reduced neuronal apoptosis and cerebral edema, and reversed RHOBTB1 and BCL2A1 dysregulation. Immune profiling showed increased monocyte/NK cell infiltration and decreased T/B lymphocytes in ICH, correlating with MitoDEGs. Flow cytometry confirmed miR-940’s role in restoring T/B cell homeostasis, and Western blotting validated key MitoDEG expression changes. This study establishes miR-940 as a key regulator of mitochondrial-immune crosstalk in ICH, modulating neuronal survival and immune microenvironment remodeling. The identified MitoDEGs and miR-940 axis may serve as potential diagnostic and therapeutic targets for ICH.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Identification of miR-940 and associated gene features as novel biomarkers for early detection of cerebral hemorrhage

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月26日

查看全文
  • XingPing Zhao,
  • HaoFang Wan,
  • Bingying Lin,
  • Inmaculada Xu Lou,
  • Shangfu Xie,
  • JianWen Guo,
  • HaiTong Wan,
  • Huifen Zhou

摘要

ICH, a severe stroke, causes neuronal death, neuroinflammation, and cerebral edema due to mitochondrial and immune dysfunction. The molecular mechanisms of secondary brain injuries are unclear, limiting effective therapies. This study used bioinformatics and experiments to explore miR-940’s role in ICH. MitoDEGs were identified via MitoCarta 3.0, and key miRNAs predicted using TargetScan and miRDB. A collagenase-induced ICH rat model with antagomir knockdown was used for validation. Neuronal damage, mitochondrial proteins, and immune cell dynamics were assessed using histopathology, qRT-PCR, Western blotting, and flow cytometry. Bioinformatics identified seven MitoDEGs and miR-940. Functional analysis linked them to mitochondrial metabolism and neuroinflammation. Inhibiting miR-940 in vivo reduced neuronal apoptosis and cerebral edema, and reversed RHOBTB1 and BCL2A1 dysregulation. Immune profiling showed increased monocyte/NK cell infiltration and decreased T/B lymphocytes in ICH, correlating with MitoDEGs. Flow cytometry confirmed miR-940’s role in restoring T/B cell homeostasis, and Western blotting validated key MitoDEG expression changes. This study establishes miR-940 as a key regulator of mitochondrial-immune crosstalk in ICH, modulating neuronal survival and immune microenvironment remodeling. The identified MitoDEGs and miR-940 axis may serve as potential diagnostic and therapeutic targets for ICH.