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- W2801144704 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 increase in AIF‑1 expression and secretion was confirmed in RAW264.7 cells in response to aldosterone. After 72 h of co‑culture between fibroblasts and macrophages stimulated with aldosterone, the α‑SMA expression was induced in fibroblasts, with significantly increased expression levels of FN and p‑p38 observed. In addition, AIF‑1 expression was reduced by stable transfection of RAW264.7 cells with AIF‑1 small interfering RNA, resulting in significantly reduced expression levels of α‑SMA, p‑p38 and FN in fibroblasts co‑cultured with macrophages as compared with normal macrophages. These findings indicate that the expression of AIF‑1 in macrophages is critical for the activation of renal fibroblasts to a profibrotic phenotype. AIF‑1 expression was upregulated in macrophages, and may be a novel mechanism linking macrophages to the promotion of RIF via the p38 signaling pathway." @default.
- W2801144704 created "2018-05-17" @default.
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- W2801144704 date "2018-05-10" @default.
- W2801144704 modified "2023-09-23" @default.
- W2801144704 title "Upregulation of allograft inflammatory factor‑1 expression and secretion by macrophages stimulated with aldosterone promotes renal fibroblasts to a profibrotic phenotype" @default.
- W2801144704 cites W1826889366 @default.
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- W2801144704 cites W1949402654 @default.
- W2801144704 cites W1965301500 @default.
- W2801144704 cites W1971972303 @default.
- W2801144704 cites W1974626393 @default.
- W2801144704 cites W1981774142 @default.
- W2801144704 cites W1982050691 @default.
- W2801144704 cites W19843932 @default.
- W2801144704 cites W1984786335 @default.
- W2801144704 cites W1990182572 @default.
- W2801144704 cites W1995127502 @default.
- W2801144704 cites W1999088219 @default.
- W2801144704 cites W2005925450 @default.
- W2801144704 cites W2009174085 @default.
- W2801144704 cites W2011121342 @default.
- W2801144704 cites W2014259212 @default.
- W2801144704 cites W2017081218 @default.
- W2801144704 cites W2019951300 @default.
- W2801144704 cites W2023848963 @default.
- W2801144704 cites W2037466124 @default.
- W2801144704 cites W2044982400 @default.
- W2801144704 cites W2060080012 @default.
- W2801144704 cites W2067956701 @default.
- W2801144704 cites W2069466601 @default.
- W2801144704 cites W2074149689 @default.
- W2801144704 cites W2074397514 @default.
- W2801144704 cites W2078657995 @default.
- W2801144704 cites W2079104440 @default.
- W2801144704 cites W2079982603 @default.
- W2801144704 cites W2082071392 @default.
- W2801144704 cites W2085999634 @default.
- W2801144704 cites W2089517445 @default.
- W2801144704 cites W2089700129 @default.
- W2801144704 cites W2101766543 @default.
- W2801144704 cites W2102815431 @default.
- W2801144704 cites W2106390653 @default.
- W2801144704 cites W2106655031 @default.
- W2801144704 cites W2107008429 @default.
- W2801144704 cites W2107277218 @default.
- W2801144704 cites W2117127436 @default.
- W2801144704 cites W2119103129 @default.
- W2801144704 cites W2125991882 @default.
- W2801144704 cites W2132526543 @default.
- W2801144704 cites W2135928448 @default.
- W2801144704 cites W2140612433 @default.
- W2801144704 cites W2141634694 @default.
- W2801144704 cites W2142480558 @default.
- W2801144704 cites W2143338501 @default.
- W2801144704 cites W2147915982 @default.
- W2801144704 cites W2155043966 @default.
- W2801144704 cites W2155602138 @default.
- W2801144704 cites W2155738377 @default.
- W2801144704 cites W2165240849 @default.
- W2801144704 cites W2165347564 @default.
- W2801144704 cites W2166890244 @default.
- W2801144704 cites W2166916539 @default.
- W2801144704 cites W2167984172 @default.
- W2801144704 cites W2170783508 @default.
- W2801144704 cites W2182604414 @default.
- W2801144704 cites W2335957989 @default.
- W2801144704 cites W2343540188 @default.
- W2801144704 cites W2405183840 @default.
- W2801144704 cites W2411149830 @default.
- W2801144704 cites W2509650855 @default.
- W2801144704 cites W2512253971 @default.
- W2801144704 cites W2587808121 @default.
- W2801144704 cites W2604833888 @default.
- W2801144704 cites W2604997718 @default.
- W2801144704 cites W2743810405 @default.
- W2801144704 cites W2788458080 @default.
- W2801144704 cites W411298156 @default.
- W2801144704 cites W4294540886 @default.
- W2801144704 cites W1964184380 @default.
- W2801144704 cites W4211127568 @default.
- W2801144704 doi "https://doi.org/10.3892/ijmm.2018.3667" @default.
- W2801144704 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6034929" @default.
- W2801144704 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29749461" @default.
- W2801144704 hasPublicationYear "2018" @default.
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