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论文题目: Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction
英文论文题目: Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction
第一作者: Tang, J; Shen, YJ; Chen, GL; Wan, QY; Wang, K; Zhang, J; Qin, J; Liu, GZ; Zuo, SK; Tao, B; Yu, Y; Wang, JW; Lazarus, M; Yu, Y
英文第一作者: Tang, J; Shen, YJ; Chen, GL; Wan, QY; Wang, K; Zhang, J; Qin, J; Liu, GZ; Zuo, SK; Tao, B; Yu, Y; Wang, JW; Lazarus, M; Yu, Y
联系作者: Yu, Y (reprint author), Univ Chinese Acad Sci, Chinese Acad Sci, Key Lab Food Safety Res, Inst Nutr Sci,Shanghai Inst Biol Sci,CAS Ctr Exce, Shanghai 200031, Peoples R China.
英文联系作者: Yu, Y (reprint author), Univ Chinese Acad Sci, Chinese Acad Sci, Key Lab Food Safety Res, Inst Nutr Sci,Shanghai Inst Biol Sci,CAS Ctr Exce, Shanghai 200031, Peoples R China.
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发表年度: 2017
卷: 8
期:
页码: 14656
摘要: Two distinct monocyte (Mo)/macrophage (Mp) subsets (Ly6C(low) and Ly6C(high)) orchestrate cardiac recovery process following myocardial infarction (MI). Prostaglandin (PG) E-2 is involved in the Mo/Mp-mediated inflammatory response, however, the role of its receptors in Mos/Mps in cardiac healing remains to be determined. Here we show that pharmacological inhibition or gene ablation of the Ep3 receptor in mice suppresses accumulation of Ly6C(low) Mos/Mps in infarcted hearts. Ep3 deletion in Mos/Mps markedly attenuates healing after MI by reducing neovascularization in peri-infarct zones. Ep3 deficiency diminishes CX3C chemokine receptor 1 (CX3CR1) expression and vascular endothelial growth factor (VEGF) secretion in Mos/Mps by suppressing TGFb1 signalling and subsequently inhibits Ly6C(low) Mos/Mps migration and angiogenesis. Targeted overexpression of Ep3 receptors in Mos/Mps improves wound healing by enhancing angiogenesis. Thus, the PGE2/Ep3 axis promotes cardiac healing after MI by activating reparative Ly6C(low) Mos/Mps, indicating that Ep3 receptor activation may be a promising therapeutic target for acute MI.
英文摘要: Two distinct monocyte (Mo)/macrophage (Mp) subsets (Ly6C(low) and Ly6C(high)) orchestrate cardiac recovery process following myocardial infarction (MI). Prostaglandin (PG) E-2 is involved in the Mo/Mp-mediated inflammatory response, however, the role of its receptors in Mos/Mps in cardiac healing remains to be determined. Here we show that pharmacological inhibition or gene ablation of the Ep3 receptor in mice suppresses accumulation of Ly6C(low) Mos/Mps in infarcted hearts. Ep3 deletion in Mos/Mps markedly attenuates healing after MI by reducing neovascularization in peri-infarct zones. Ep3 deficiency diminishes CX3C chemokine receptor 1 (CX3CR1) expression and vascular endothelial growth factor (VEGF) secretion in Mos/Mps by suppressing TGFb1 signalling and subsequently inhibits Ly6C(low) Mos/Mps migration and angiogenesis. Targeted overexpression of Ep3 receptors in Mos/Mps improves wound healing by enhancing angiogenesis. Thus, the PGE2/Ep3 axis promotes cardiac healing after MI by activating reparative Ly6C(low) Mos/Mps, indicating that Ep3 receptor activation may be a promising therapeutic target for acute MI.
刊物名称: NATURE COMMUNICATIONS
英文刊物名称: NATURE COMMUNICATIONS
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学科: Multidisciplinary Sciences
英文学科: Multidisciplinary Sciences
影响因子: 12.124
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论文类别: Article
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