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论文题目: PKA regulatory II alpha subunit is essential for PGD(2)-mediated resolution of inflammation
英文论文题目: PKA regulatory II alpha subunit is essential for PGD(2)-mediated resolution of inflammation
第一作者: Kong, DP; Shen, YJ; Liu, GZ; Zuo, SK; Ji, Y; Lu, AK; Nakamura, M; Lazarus, M; Stratakis, CA; Breyer, RM; Yu, Y
英文第一作者: Kong, DP; Shen, YJ; Liu, GZ; Zuo, SK; Ji, Y; Lu, AK; Nakamura, M; Lazarus, M; Stratakis, CA; Breyer, RM; Yu, Y
联系作者: Yu, Y (reprint author), Univ Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Food Safety Res,CAS Ctr Excellence Mol Ce, Shanghai 200031, Peoples R China.
英文联系作者: Yu, Y (reprint author), Univ Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Food Safety Res,CAS Ctr Excellence Mol Ce, Shanghai 200031, Peoples R China.
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发表年度: 2016
卷: 213
期: 10
页码: 2209-2226
摘要: The kinetic participation of macrophages is critical for inflammatory resolution and recovery from myocardial infarction (MI), particularly with respect to the transition from the M1 to the M2 phenotype; however, the underlying mechanisms are poorly understood. In this study, we found that the deletion of prostaglandin (PG) D-2 receptor subtype 1 (DP1) in macrophages retarded M2 polarization, antiinflammatory cytokine production, and resolution in different inflammatory models, including the MI model. DP1 deletion up-regulated proinflammatory genes expression via JAK2/STAT1 signaling in macrophages, whereas its activation facilitated binding of the separated PKA regulatory IIa subunit (PRK AR2A) to the transmembrane domain of IFN-gamma receptor, suppressed JAK2-STAT1 axis-mediated M1 polarization, and promoted resolution. PRK AR2A deficiency attenuated DP1 activation-mediated M2 polarization and resolution of inflammation. Collectively, PGD(2)-DP1 axis-induced M2 polarization facilitates resolution of inflammation through the PRK AR2A-mediated suppression of JAK2/STAT1 signaling. These observations indicate that macrophage DP1 activation represents a promising strategy in the management of inflammation- associated diseases, including post-MI healing.
英文摘要: The kinetic participation of macrophages is critical for inflammatory resolution and recovery from myocardial infarction (MI), particularly with respect to the transition from the M1 to the M2 phenotype; however, the underlying mechanisms are poorly understood. In this study, we found that the deletion of prostaglandin (PG) D-2 receptor subtype 1 (DP1) in macrophages retarded M2 polarization, antiinflammatory cytokine production, and resolution in different inflammatory models, including the MI model. DP1 deletion up-regulated proinflammatory genes expression via JAK2/STAT1 signaling in macrophages, whereas its activation facilitated binding of the separated PKA regulatory IIa subunit (PRK AR2A) to the transmembrane domain of IFN-gamma receptor, suppressed JAK2-STAT1 axis-mediated M1 polarization, and promoted resolution. PRK AR2A deficiency attenuated DP1 activation-mediated M2 polarization and resolution of inflammation. Collectively, PGD(2)-DP1 axis-induced M2 polarization facilitates resolution of inflammation through the PRK AR2A-mediated suppression of JAK2/STAT1 signaling. These observations indicate that macrophage DP1 activation represents a promising strategy in the management of inflammation- associated diseases, including post-MI healing.
刊物名称: JOURNAL OF EXPERIMENTAL MEDICINE
英文刊物名称: JOURNAL OF EXPERIMENTAL MEDICINE
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学科: Immunology; Medicine, Research & Experimental
英文学科: Immunology; Medicine, Research & Experimental
影响因子: 11.991
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论文类别: Article
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