2010
DOI: 10.1172/jci41080
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Myeloid mineralocorticoid receptor controls macrophage polarization and cardiovascular hypertrophy and remodeling in mice

Abstract: Inappropriate excess of the steroid hormone aldosterone, which is a mineralocorticoid receptor (MR) agonist, is associated with increased inflammation and risk of cardiovascular disease. MR antagonists are cardioprotective and antiinflammatory in vivo, and evidence suggests that they mediate these effects in part by aldosterone-independent mechanisms. Here we have shown that MR on myeloid cells is necessary for efficient classical macrophage activation by proinflammatory cytokines. Macrophages from mice lackin… Show more

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Cited by 336 publications
(385 citation statements)
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“…2009; Usher et al. 2010), our data support the notion that EC‐MR does not regulate cardiac fibrosis, but rather that MR in infiltrating leukocytes likely mediates this profibrotic effect. Indeed, we demonstrate that leukocyte infiltration in perivascular areas colocalize with perivascular fibrosis in EC‐MR −/− and EC‐MR +/+ mice.…”
Section: Discussionsupporting
confidence: 82%
“…2009; Usher et al. 2010), our data support the notion that EC‐MR does not regulate cardiac fibrosis, but rather that MR in infiltrating leukocytes likely mediates this profibrotic effect. Indeed, we demonstrate that leukocyte infiltration in perivascular areas colocalize with perivascular fibrosis in EC‐MR −/− and EC‐MR +/+ mice.…”
Section: Discussionsupporting
confidence: 82%
“…In comparison, studies in models of CVD and cerebral ischemia have shown that MyMRKO mice have reduced levels of M1 cytokines and that this can occur with and without a reduction in macrophage numbers. 15,16,19 Notably, some of these in vivo studies and experiments using cultured cells have indicated that a deficiency of MR signaling in macrophages can alter macrophage gene expression toward an M2 alternatively activated phenotype. 15,16 Our PCR analysis of CD11b + macrophages isolated from WT and MyMRKO kidneys at day 15 of disease found no difference in the M1/M2 phenotype.…”
Section: Discussionmentioning
confidence: 99%
“…15,16,19 Notably, some of these in vivo studies and experiments using cultured cells have indicated that a deficiency of MR signaling in macrophages can alter macrophage gene expression toward an M2 alternatively activated phenotype. 15,16 Our PCR analysis of CD11b + macrophages isolated from WT and MyMRKO kidneys at day 15 of disease found no difference in the M1/M2 phenotype. Thus, the difference in expression of most of these markers in the diseased kidneys is probably due to changes in macrophage numbers rather than in their phenotype.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…6b). To further examine the effects of Retnla deficiency on macrophage phenotypes in vitro, we analysed the M1/M2 markers in peritoneal macrophages from Retnla À / À and WT mice using well-established M1 (lipopolysaccharide; LPS) or M2 (IL-4) polarizing agents 39 . Expression of M1/M2 genes in Retnla À / À microphages did not differ from those of WT macrophages in either the absence or presence of LPS or IL-4 ( Supplementary Fig.…”
Section: Resultsmentioning
confidence: 99%