TIMP-1通过诱导Fli-1促进实验性肝纤维化中MCP-1的表达和巨噬细胞的迁移

核心信息

  • 论文英文标题: TIMP-1 Promotes Expression of MCP-1 and Macrophage Migration by Inducing Fli-1 in Experimental Liver Fibrosis
  • 期刊: J Clin Transl Hepatol
  • 发表年份: 2024
  • DOI: 10.14218/JCTH.2023.00514
  • PMID/PMCID: 38993513; PMC11233975

研究概览

This study aimed to explore the pathways through which TIMP-1 controls monocyte chemoattractant protein-1 (MCP-1) expression and promotes hepatic macrophage recruitment. This study aimed to explore the pathways through which TIMP-1 controls monocyte chemoattractant protein-1 (MCP-1) expression and promotes hepatic macrophage recruitment.

核心发现

siRNA-TIMP-1 alleviated carbon tetrachloride-induced liver fibrosis, reducing macrophage migration and MCP-1 expression.

Co-culturing macrophages with hepatic stellate cells (HSCs) post-TIMP-1 downregulation inhibited macrophage migration.

In siRNA-TIMP-1-treated HSCs, microRNA-145 (miRNA-145) expression increased, while the expression of Friend leukemia virus integration-1 (Fli-1) and MCP-1 was inhibited.

Downregulation of Fli-1 led to decreased MCP-1 expression, whereas Fli-1 overexpression increased MCP-1 expression within HSCs.

研究设计

Liver fibrosis was triggered through carbon tetrachloride, and an adeno-associated virus containing small interfering RNA targeting TIMP-1 (siRNA-TIMP-1) was administered to both rats and mice.

We assessed the extent of fibrosis and macrophage recruitment.

The molecular mechanisms regulating macrophage recruitment by TIMP-1 were investigated through transwell migration assays, luciferase reporter assays, the use of pharmacological modulators, and an analysis of extracellular vesicles (EVs).

Echo Biotech 角色

外泌体分离鉴定&外泌体和细胞miRNA测序分析

关联平台: Exoomics®

关联服务与能力: EV Isolation & Purification, EV Basic Characterization (TEM/NTA/WB), EV miRNA Profiling / Sequencing

关联产品或试剂: 无明确产品引用

参考文献

原始论文: TIMP-1 Promotes Expression of MCP-1 and Macrophage Migration by Inducing Fli-1 in Experimental Liver Fibrosis Journal of clinical and translational hepatology. 2024. DOI: 10.14218/JCTH.2023.00514. PMID/PMCID: 38993513; PMC11233975.