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Anti‐liver fibrotic effect of triggering receptor expressed on myeloid cells 2 (TREM2) via macrophage phenotype switching
Author(s) -
Kang Byeongseok,
Kim Nayoun,
Yang Jin Won,
Kang Keon Wook
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.563.1
Subject(s) - trem2 , hepatic stellate cell , biology , myeloid , macrophage , hepatic fibrosis , receptor , genetically modified mouse , fibrosis , phenotype , cancer research , endocrinology , transgene , medicine , in vitro , myeloid cells , biochemistry , gene
Macrophage phenotype switching is critical for the progress of inflammatory diseases. The aim of this study is to investigate the potential role of triggering receptor expressed on myeloid cells‐2 (TREM2) in macrophage phenotype switching and liver fibrosis. TREM2 protein expression was increased in fibrotic livers from human and mouse. Transforming growth factor‐β1 (TGFβ1), a representative stimulus for the differentiation of M2c macrophage, specifically increased TREM2 expression in Raw264.7 macrophage cells. Co‐culture of hepatic stellate cells (HSCs) with TREM2‐overexpressing Raw264.7 cells showed the decreased expression of IL‐6 compared to co‐culture of HSCs and mock‐Raw264.7 cells. TREM2‐transgenic mice showed the decreased liver fibrosis in CCl 4 ‐induced liver fibrosis model, whereas TREM2‐null mice showed the aggravated liver fibrosis compared to wild‐type mice. The basal mRNA level of interleukin‐10 was enhanced and the basal level of monocyte chemoattractant protein‐1 was decreased in liver samples from TREM2‐transgenic mice. Therefore, the overexpressed TREM2 in macrophages from fibrotic liver suppresses the progress of hepatic fibrogenesis. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .