Upregulation of allograft inflammatory factor‑1 expression and secretion by macrophages stimulated with aldosterone promotes renal fibroblasts to a profibrotic phenotype

International Journal of Molecular Medicine
Yushu LiLirong Hao

Abstract

Macrophages have been identified as a key cell type in the pathogenesis of renal interstitial fibrosis (RIF). However, the mechanism through which macrophages drive fibrosis remains unclear. The current study focuses on the effects and possible underlying mechanism of allograft inflammatory factor‑1 (AIF‑1), an inflammation‑responsive scaffold protein expressed and secreted by macrophages, in promoting fibroblasts to a profibrotic phenotype. In vivo experiments indicated that AIF‑1, CD68 and α‑smooth muscle actin (α‑SMA) were upregulated in kidney tissues of mice subjected to unilateral ureteric obstruction, while their expressions were inhibited by an aldosterone receptor antagonist, spironolactone. Double immunofluorescence staining revealed that AIF‑1 expression co‑localized with CD68‑positive macrophages in the renal interstitium, indicating that AIF‑1 expression in macrophages was increased in the RIF animal model. Furthermore, to identify the role of AIF‑1 in promoting fibrosis, its expression and secretion by the RAW264.7 macrophage cell line were detected in vitro. The expression levels of α‑SMA, phosphorylated p38 (p‑p38) and fibronectin (FN) in fibroblasts were examined subsequent to co‑culture with macrophages. The i...Continue Reading

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Methods Mentioned

BETA
biopsies
fluorescence microscopy
transfection
protein assay
ELISA

Software Mentioned

SPSS

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