Folic acid-mediated fibrosis is driven by C5a receptor 1-mediated activation of kidney myeloid cells.

ABSTRACT: We have previously reported that increased expression and activation of kidney cell complement components play an important role in the pathogenesis of renal scarring. Here, we used floxed green fluorescent protein (GFP)-C5a receptor 1 (C5aR1) knockin mice (GFP-C5ar1^fl/fl) and the model of folic acid (FA)-induced kidney injury to define the cell types and potential mechanisms by which increased C5aR1 activation leads to fibrosis. Using flow cytometry and confocal microscopy, we identified macrophages as the major interstitial cell type showing increased expression of C5aR1 in FA-treated mice. C5ar1^fl/fl.Lyz2Cre^+/- mice, in which C5aR1 has been specifically deleted in lysozyme M-expressing myeloid cells, experienced reduced fibrosis comp

SUBMITTER: Sahu RK 

PROVIDER: S-EPMC9054266 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature