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Chemerin/ChemR23 signaling axis is involved in the endothelial protection by KATP channel opener iptakalim

  
@article{APS5463,
	author = {Rui-jun Zhao and Hai Wang},
	title = {Chemerin/ChemR23 signaling axis is involved in the endothelial protection by KATP channel opener iptakalim},
	journal = {Acta Pharmacologica Sinica},
	volume = {32},
	number = {5},
	year = {2016},
	keywords = {},
	abstract = {Aim: To elucidate the modulation of the chemerin/ChemR23 axis by iptakalim-induced opening of KATP channels and to determine the role of the chemerin/ChemR23 axis in the iptakalim-mediated endothelial protection.
 Methods: Cultured rat aortic endothelial cells (RAECs) were used. Chemerin secretion and ChemR23 protein expression were investigated using Western blot analysis. The gene expression level of ChemR23 was examined with RT-PCR. In addition, the release of nitric oxide (NO) was measured with a nitric oxide assay.
 Results: Homocysteine, uric acid, high glucose, or oxidized low-density lipoprotein (ox-LDL) down-regulated the chemerin secretion and ChemR23 gene/protein expression in RAECs as a function of concentration and time, which was reversed by pretreatment with iptakalim (1-10 μmol/L). Moreover, these effects of iptakalim were abolished in the presence of the KATP channel antagonist glibenclamide (1 μmol/L). Both iptakalim and recombinant chemerin restored the impaired NO production in RAECs induced by uric acid, and the effects were abolished by anti-ChemR23 antibodies.
 Conclusion: Iptakalim via opening KATP channels enhanced the endothelial chemerin/ChemR23 axis and NO production, thus improving endothelial function.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/5463}
}