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Catalase potentiates retinoic acid‐induced THP‐1 monocyte differentiation into macrophage through inhibition of peroxisome proliferator‐activated receptor γ
Author(s) -
Ding Qiurong,
Jin Ting,
Wang Zhenzhen,
Chen Yan
Publication year - 2007
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1106672
Subject(s) - retinoic acid , peroxisome proliferator activated receptor , catalase , biology , thp1 cell line , monocyte , cellular differentiation , retinoic acid receptor , macrophage , receptor , microbiology and biotechnology , biochemistry , cell culture , immunology , enzyme , genetics , gene , in vitro
Macrophage differentiation plays a pivotal role in cardiovascular diseases and many other physiological processes. However, the role of reaction oxygen species in macrophage differentiation has not been elucidated. Here, we report functional characterization of catalase, an enzyme that degrades hydrogen peroxide (H 2 O 2 ), in THP‐1 monocyte differentiation. Treatment of THP‐1 cells with catalase was able to synergize with all‐trans retinoic acid (ATRA) to enhance macrophage differentiation, demonstrated by changes of cell adherence, cell cycle arrest, nitroblue tetrazolium reduction, and expression of differentiation markers including CD68, CD11b, and matrix metalloproteinase 9 (MMP9). ATRA could stimulate retinoic acid (RA) receptor‐mediated transcription, but this was not affected by catalase. However, ATRA and catalase were capable of reducing transcriptional activity mediated by peroxisome proliferator‐activated receptor γ (PPARγ). Consistently, PPARγ antagonists enhanced, and PPARγ agonists inhibited MMP9 expression stimulated by ATRA and catalase in THP‐1 cells. Therefore, these data indicate that catalase is able to potentiate ATRA‐induced macrophage differentiation by inhibition of PPARγ activity, underscoring an important interplay between H 2 O 2 , RA, and PPARγ in macrophages.