USP7-mediated stabilization of CXCL3 aggravates inflammation in models of acute lung injury.

ABSTRACT:

Background

CXCL3 is involved in the pathogenesis of asthmatic lungs; however, its specific function in sepsis-induced acute lung injury (ALI) remains unclear. This study aimed to elucidate the modulatory function of CXCL3 and its relationship to the deubiquitinating enzyme USP7 in lung inflammation. As model systems, we used lipopolysaccharide (LPS) stimulation of human lung microvascular endothelial cells (HLMVECs) and macrophages in vitro and a mouse model of sepsis-induced ALI.

Methods

Cell behavior was assessed using Cell Counting Kit-8, 5-Ethynyl-2'-deoxyuridine assays, flow cytometry, biochemical, and Western blotting assays. STAT3-binding sites on CXCL3 were predicted via the JASPAR database. Interactions between CXCL3, STAT3, and USP7 were confirmed through chromatin

SUBMITTER: Lv H 

PROVIDER: S-EPMC12557704 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature