小鼠心脏缝隙连接蛋白节律性表达与生物钟系统相关性

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Abstract Objective: To examine the circadian expression of cardiac connexin genes in the mouse and its correlation with biological clock. Methods: After 2-week constant housing, the atrium and ventricle of wild and Clock mutant mice were sampled every 6 hours. The expressions of Clock genes (Per2 and Dbp), cardiac connexin genes (Cx40 and Cx43) were determined by the real-time quantitative PCR. Results: The mRNA levels of all examined genes showed substantial circadian rhythms in wild type mice. In clock mutant mice, Per2 and Dbp lost circadian rhythms in both atrium and ventricle, while Cx40 and Cx43 still had circadian rhythms but phase-shifted significantly, which were phase-advanced in atrium and phase-delayed in ventricle. The Cx40, Cx43 expressions were upregulated in ventricle. Conclusion: Cardiac Cx40 and Cx43 gene expressions shows clear circadian rhythm in mice and may be associated with the biological clock system.

Key words： connexin Clock mutant circadian rhythm mice

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	Articles by authors
	CHAI Ying
	ZHOU Ying
	CHEN Xiaomin
	TONG Maoqing

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https://xb.wmu.edu.cn/EN/ OR https://xb.wmu.edu.cn/EN/Y2018/V48/I1/42

[1] YAMASHITA T, SEKIGUCHI A, IWASAKI Y K, et al. Circadian variation of cardiac K+ channel gene expression[J]. Circulation, 2003, 107(14): 1917-1922.

[2] TONG M, WATANABE E, YAMAMOTO N, et al. Circadian expressions of cardiac ion channel genes in mouse might be associated with the central clock in the SCN but not the peripheral clock in the heart[J]. Biological Rhythm Research, 2013, 44(4): 519-530.

[3] DELMAR M, MAKITA N. Cardiac connexins, mutations and arrhythmias[J]. Curr Opin Cardiol, 2012, 27(3): 236-241.

[4] OSBOURNE A, CALWAY T, BROMAN M, et al. Downregulation of connexin43 by microRNA-130a in cardiomyocytes results in cardiac arrhythmias[J]. J Mol Cell Cardiol, 2014, 74: 53-63.

[5] JANSEN J A, VAN VEEN T A, DE BAKKER J M, et al. Cardiac connexins and impulse propagation[J]. J Mol Cell Cardiol, 2010, 48(1): 76-82.

[6] SHIN S Y, JO W M, MIN T J, et al. Gap junction remodelling by chronic pressure overload is related to the increased susceptibility to atrial fibrillation in rat heart[J]. Europace, 2015, 17(4): 655-663.

[7] ZICHA J, PECHANOVA O, CACANYIOVA S, et al. Hereditary hypertriglyceridemic rat: a suitable model of cardiovascular disease and metabolic syndrome?[J]. Physiol Res, 2006, 55(Suppl 1): 49-63.

[8] SCHEER F A, TER HORST G J, VAN DER VLIET J, et al. Physiological and anatomic evidence for regulation of the heart by suprachiasmatic nucleus in rats[J]. Am J Physiol Heart Circ Physiol, 2001, 280(3): 1391-1399.

[9] LESAUTER J, SILVER R. Output signals of the SCN[J]. Chronobiol Int, 1998, 15: 535-550.

[10] TAKEDA N, MAEMURA K. Circadian clock and the onset of cardiovascular events[J]. Hypertens Res, 2016, 39(6): 383-90.

[11] INGLE K A, KAIN V, GOEL M, et al. Cardiomyocyte-specific Bmal1 deletion in mice triggers diastolic dysfunction, extracellular matrix response, and impaired resolution of inflammation[J]. Am J Physiol Heart Circ Physiol, 2015, 309(11): 1827-1836.

[12] HAVAKUK O, ZUKERMAN N, FLINT N, et al. Shift work and the risk of coronary artery disease: A cardiac computed tomography angiography study[J]. Cardiology, 2017, 139(1): 11-16.

[13] YOUNG M E, WILSON C R, RAZEGHI P, et al. Alterations of the circadian clock in the heart by streptozotocin-induced diabetes[J]. J Mol Cell Cardiol, 2002, 34(2): 223-231.