学術雑誌論文 Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction

Tang, Juan  ,  Shen, Yujun  ,  Chen, Guilin  ,  Wan, Qiangyou  ,  Wang, Kai  ,  Zhang, Jian  ,  Qin, Jing  ,  Liu, Guizhu  ,  Zuo, Shengkai  ,  Tao, Bo  ,  Yu, Yu  ,  Wang, Junwen  ,  Lazarus, Michael  ,  Yu, Ying

8p.14656 , 2017-03 , Nature Publishing Group
ISSN:2041-1723
NII書誌ID(NCID):AA12645905
内容記述
Two distinct monocyte (Mo)/macrophage (Mp) subsets (Ly6Clow and Ly6Chigh) orchestrate cardiac recovery process following myocardial infarction (MI). Prostaglandin (PG) E2 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 Ly6Clow 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 TGFβ1 signalling and subsequently inhibits Ly6Clow 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 Ly6Clow Mos/Mps, indicating that Ep3 receptor activation may be a promising therapeutic target for acute MI.
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