Macrophage migration inhibitory factor mediates joint capsule fibrosis via facilitating phospholipid metabolite PGE2 production in fibroblasts.

ABSTRACT:

Background

Joint capsule persistent inflammation and subsequent fibrosis lead to post-traumatic joint contracture (PTJC). Fibroblasts, as a bridge between inflammation and fibrosis, participate in regulating the pathological microenvironment after injury. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that can be inducibly expressed in lesioned joint capsule, yet its role in regulating fibroblast function to tune milieu following PTJC remains elusive.

Methods

The influence of MIF on the expression of phospholipid metabolite prostaglandin E2 (PGE2) and relevant pathways were investigated using qRT-PCR, Western blot, ELISA, EdU, Transwell, siRNA, and immunofluorescence following establishment of rat PTJC model, fibroblast model, and macrophage model

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC12276190 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature