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Transducin‐like enhancer of split‐1 is expressed and functional in human macrophages
Author(s) -
De Paoli Federica,
Copin Corinne,
Vanhoutte Jonathan,
Derudas Bruno,
Vinod Manjula,
Zawadzki Christophe,
Susen Sophie,
Pattou François,
Haulon Stéphan,
Staels Bart,
Eeckhoute Jérome,
ChinettiGbaguidi Giulia
Publication year - 2016
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12029
Subject(s) - proinflammatory cytokine , enhancer , microbiology and biotechnology , corepressor , macrophage polarization , phenotype , adipose tissue macrophages , macrophage activating factor , gene silencing , lipopolysaccharide , macrophage , in vitro , adipose tissue , chemistry , biology , inflammation , immunology , gene expression , genetics , biochemistry , gene , repressor , white adipose tissue
Macrophages display heterogeneous phenotypes, including the classical M1 proinflammatory and the alternative M2 anti‐inflammatory polarization states. The transducin‐like enhancer of split‐1 ( TLE 1) is a transcriptional corepressor whose functions in macrophages have not been studied yet. We report that TLE 1 is highly expressed in human alternative macrophages in vitro and in atherosclerotic plaques as well as in adipose tissue M1/M2 mixed macrophages. TLE 1 silencing in alternative macrophages decreases the expression of the M2 markers IL ‐1Ra and IL ‐10 , while it exacerbates TNF α and CCL 3 induction by lipopolysaccharide. Hence, TLE 1 is expressed in human macrophages where it has potential anti‐inflammatory and alternative phenotype promoting properties.