C1 q/tumor necrosis factor-related protein-3 enhances the contractility   of cardiomyocyte by increasing calcium sensitivity

doi:10.1016/j.ceca.2017.06.009

CORC > 北京大学 > 生命科学学院

	C1 q/tumor necrosis factor-related protein-3 enhances the contractility of cardiomyocyte by increasing calcium sensitivity
	Zhang, Cheng-Lin ; Chen, Zheng-Ju ; Feng, Han ; Zhao, Qian ; Cao, Yang-Po ; Li, Li ; Wang, Jin-Yu ; Zhang, Yan ; Wu, Li-Ling
刊名	CELL CALCIUM
	2017
关键词	Cloitumor necrosis factor-related protein-3 Contraction Ca2+ transient Ca2+ sensitivity RAT VENTRICULAR MYOCYTES TROPONIN-I PHOSPHORYLATION CARDIAC MYOCYTES ADIPOSE-TISSUE INSULIN-RESISTANCE SIGNALING PATHWAY HEART-FAILURE CA2+ CURRENT OBESE MICE ACTIVATION
DOI	10.1016/j.ceca.2017.06.009
英文摘要	C1q/tumor necrosis factor-related protein-3 (CTRP3) is an adipokine that protects against myocardial infarction-induced cardiac dysfunction through its pro-angiogenic, anti-apoptotic, and anti-fibrotic effects. However, whether CTRP3 can directly affect the systolic and diastolic function of cardiomyocytes remains unknown. Adult rat cardiomyocytes were isolated and loaded with Fura-2AM. The contraction and Ca2+ transient data was collected and analyzed by lonOptix system. 1 and 2 mu g/ml CTRP3 significantly increased the contraction of cardiomyocytes. However, CTRP3 did not alter the diastolic Ca2+ content, systolic Ca2+ content, Ca2+ transient amplitude, and L-type Ca2+ channel current. To reveal whether CTRP3 affects the Ca2+ sensitivity of cardiomyocytes, the typical phase-plane diagrams of sarcomere length vs. Fura-2 ratio was performed. We observed a left-ward shifting of the late relaxation trajectory after CTRP3 perfusion, as quantified by decreased Ca2+ content at 50% sarcomere relaxation, and increased mean gradient (mu m/Fura-2 ratio) during 500-600ms (-0.163 vs. 0.279), 500-700 ms (-0.159 vs. 0.248), and 500-800 ms (-0.148 vs. 0.243). Consistently, the phosphorylation level of cardiac troponin I at Ser23/24 was reduced by CTRP3, which could be eliminated by preincubation of okadaic acid, a type 2A protein phosphatase inhibitor. In summary, CTRP3 increases the contraction of cardiomyocytes by increasing the myofilament Ca2+ sensitivity. CTRP3 might be a potential endogenous Ca2+ sensitizer that modulates the contractility of cardiomyocytes. (C) 2017 Elsevier Ltd. All rights reserved.; National Natural Science Foundation of China [81470398, 81170974, 81370192]; SCI(E); ARTICLE; 90-97; 66
语种	英语
内容类型	期刊论文
源URL	[http://ir.pku.edu.cn/handle/20.500.11897/471122]
专题	生命科学学院
推荐引用方式 GB/T 7714	Zhang, Cheng-Lin,Chen, Zheng-Ju,Feng, Han,et al. C1 q/tumor necrosis factor-related protein-3 enhances the contractility of cardiomyocyte by increasing calcium sensitivity[J]. CELL CALCIUM,2017.
APA	Zhang, Cheng-Lin.,Chen, Zheng-Ju.,Feng, Han.,Zhao, Qian.,Cao, Yang-Po.,...&Wu, Li-Ling.(2017).C1 q/tumor necrosis factor-related protein-3 enhances the contractility of cardiomyocyte by increasing calcium sensitivity.CELL CALCIUM.
MLA	Zhang, Cheng-Lin,et al."C1 q/tumor necrosis factor-related protein-3 enhances the contractility of cardiomyocyte by increasing calcium sensitivity".CELL CALCIUM (2017).