Urokinase plasminogen activator induces pro-fibrotic/m2 phenotype in murine cardiac macrophages.

ABSTRACT:

Objective

Inflammation and fibrosis are intertwined in multiple disease processes. We have previously found that over-expression of urokinase plasminogen activator in macrophages induces spontaneous macrophage accumulation and fibrosis specific to the heart in mice. Understanding the relationship between inflammation and fibrosis in the heart is critical to developing therapies for diverse myocardial diseases. Therefore, we sought to determine if uPA induces changes in macrophage function that promote cardiac collagen accumulation.

Methods and results

We analyzed the effect of the uPA transgene on expression of pro-inflammatory (M1) and pro-fibrotic (M2) genes and proteins in hearts and isolated macrophages of uPA overexpressing mice. We found that although there was elevati

SUBMITTER: Meznarich J 

PROVIDER: S-EPMC3594198 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature