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Beta‐catenin promotes macrophage‐mediated acute inflammatory response after myocardial infarction
Author(s) -
Huang Ling,
Xiang Mei,
Ye Ping,
Zhou Wei,
Chen Manhua
Publication year - 2018
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1111/imcb.1019
Subject(s) - proinflammatory cytokine , inflammation , macrophage , adoptive cell transfer , myocardial infarction , catenin , cancer research , medicine , beta catenin , microbiology and biotechnology , wnt signaling pathway , immunology , signal transduction , chemistry , biology , immune system , in vitro , t cell , biochemistry
Regulatory mechanisms for acute inflammatory responses post myocardial infarction ( MI ) have yet to be fully understood. In particular, the mechanisms by which cardiac macrophages modulate MI ‐induced myocardial inflammation remains unclear. In this study, using a mouse MI model, we showed that β‐catenin‐mediated signaling was activated in cardiac macrophages post‐ MI , especially in Ly‐6C‐positive proinflammatory macrophages. Using a RAW 264.7‐based β‐catenin reporter cell line, we confirmed the presence of active β‐catenin and its downstream signaling in cardiac macrophages after MI . Moreover, lentivirus‐mediated inducible expression of constitutively active β‐catenin revealed that β‐catenin plays a role in promoting the inflammatory response by RAW 264.7 cells. Depletion of endogenous macrophages and adoptive transfer of active β‐catenin‐expressing RAW 264.7 cells resulted in enhancement of acute myocardial inflammation in recipient mice after MI , as demonstrated by elevated levels of lymphocyte infiltrates and increased expression of proinflammatory cytokines. However, infarct volume, myocardial tissue repair, and left ventricle function were not influenced by the expression of active β‐catenin in the adoptive transfer assay. Our research has demonstrated that β‐catenin‐mediated signaling is important for cardiac macrophages to modulate post‐ MI inflammatory responses. These findings may be valuable for developing novel therapeutic strategies for MI .