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miRNA-711-SP1-胶原I型信号通路参与吡格列酮抗心肌梗死后心脏纤维化作用

, PP. 464-472

Keywords: 吡格列酮,miR-711,心脏纤维化

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Abstract:

microRNAs在心脏纤维化中的作用已被广泛研究,但药物调控microRNAs发挥抗纤维化作用及其机制尚不明确.研究显示,吡格列酮能改善心脏纤维化,促进miR-711表达.本研究旨在阐明心肌梗死后吡格列酮改变miR-711表达产生的效应及其机制.结果提示,吡格列酮减少心肌梗死后I型胶原表达,上调miR-711表达.心脏成纤维细胞中,吡格列酮促进miR-711表达,过表达miR-711抑制I型胶原表达.阻抑miR-711,吡格列酮下调的I型胶原表达升高.生物信息学筛选SP1为miR-711的靶基因,经荧光素酶报告基因实验及Westernblot验证.此外,吡格列酮降低心肌梗死后SP1的表达量,成纤维细胞转染antagomir-711后,吡格列酮下调的SP1表达量升高.本研究发现,miR-711-SP1-I型胶原信号途径参与吡格列酮抗纤维化效应,为基于miRNAs的药物研究提供新的策略.

References

[1]  1 Opie L H, Commerford P J, Gersh B J, et al. Controversies in ventricular remodelling. Lancet, 2006, 367: 356-367
[2]  2 Biswas A, Rabbani S I, Devi K. Influence of pioglitazone on experimental heart failure and hyperlipidemia in rats. Indian J Pharmacol, 2012, 44: 333-339
[3]  3 Kataoka Y, Yagi N, Kokubu N, et al. Effect of pretreatment with pioglitazone on reperfusion injury in diabetic patients with acute myocardial infarction. Circ J, 2011, 75: 1968-1974
[4]  4 Shiomi T, Tsutsui H, Hayashidani S, et al. Pioglitazone, a peroxisome proliferator-activated receptor-gamma agonist, attenuates left ventricular remodeling and failure after experimental myocardial infarction. Circulation, 2002, 106: 3126-3132
[5]  5 Wayman N S, Hattori Y, Mcdonald M C, et al. Ligands of the peroxisome proliferator-activated receptors (PPAR-gamma and PPAR- alpha) reduce myocardial infarct size. FASEB J, 2002, 16: 1027-1040
[6]  8 van Rooij E, Sutherland L B, Thatcher J E, et al. Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis. Proc Natl Acad Sci USA, 2008, 105: 13027-13032
[7]  9 Cheng K, Malliaras K, Shen D, et al. Intramyocardial injection of platelet gel promotes endogenous repair and augments cardiac function in rats with myocardial infarction. J Am Coll Cardiol, 2012, 59: 256-264
[8]  10 Simpson P, Savion S. Differentiation of rat myocytes in single cell cultures with and without proliferating nonmyocardial cells. Cross-striations, ultrastructure, and chronotropic response to isoproterenol. Circ Res, 1982, 50: 101-116
[9]  11 Caglayan E, Stauber B, Collins A R, et al. Differential roles of cardiomyocyte and macrophage peroxisome proliferator-activated receptor gamma in cardiac fibrosis. Diabetes, 2008, 57: 2470-2479
[10]  6 Yasuda S, Kobayashi H, Iwasa M, et al. Antidiabetic drug pioglitazone protects the heart via activation of PPAR-gamma receptors, PI3-kinase, Akt, and eNOS pathway in a rabbit model of myocardial infarction. Am J Physiol Heart Circ Physiol, 2009, 296: H1558-H1565
[11]  7 Mohite A J, Chillar A J, Wijaya C, et al. Endogenous prostacyclin signaling regulating microRNA expression in mammalian cells. FASEB J, 2009, 23: LB373
[12]  12 Zhao S M, Shen L H, Li H W, et al. Down-regulation of the expression of angiotensin II type 1 receptor in neonatal rat cardiac fibroblast by activation of PPARgamma signal pathway. Chin J Physiol, 2008, 51: 357-362
[13]  13 Nakamura T, Yamamoto E, Kataoka K, et al. Beneficial effects of pioglitazone on hypertensive cardiovascular injury are enhanced by combination with candesartan. Hypertension, 2008, 51: 296-301
[14]  14 Elrashidy R A, Asker M E, Mohamed H E. Pioglitazone attenuates cardiac fibrosis and hypertrophy in a rat model of diabetic nephropathy. J Cardiovasc Pharmacol Ther, 2012, 17: 324-333
[15]  15 Yu Y, Zhang Z H, Wei S G, et al. Peroxisome proliferator-activated receptor-gamma regulates inflammation and renin-angiotensin system activity in the hypothalamic paraventricular nucleus and ameliorates peripheral manifestations of heart failure. Hypertension, 2012, 59: 477-484
[16]  16 Han S, Rivera H N, Roman J. Peroxisome proliferator-activated receptor-gamma ligands inhibit alpha5 integrin gene transcription in non-small cell lung carcinoma cells. Am J Respir Cell Mol Biol, 2005, 32: 350-359
[17]  17 Grohe C, Kahlert S, Lobbert K, et al. Angiotensin converting enzyme inhibition modulates cardiac fibroblast growth. J Hypertens, 1998, 16: 377-384
[18]  18 Redell J B, Liu Y, Dash P K. Traumatic brain injury alters expression of hippocampal microRNAs: potential regulators of multiple pathophysiological processes. J Neurosci Res, 2009, 87: 1435-1448
[19]  19 Wang K, Zhang S, Marzolf B, et al. Circulating microRNAs, potential biomarkers for drug-induced liver injury. Proc Natl Acad Sci USA, 2009, 106: 4402-4407
[20]  20 Creemers E E, Pinto Y M. Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart. Cardiovasc Res, 2011, 89: 265-272
[21]  21 Inagaki Y, Nemoto T, Nakao A, et al. Interaction between GC box binding factors and Smad proteins modulates cell lineage-specific alpha 2(I) collagen gene transcription. J Biol Chem, 2001, 276: 16573-16579
[22]  22 Poncelet A C, Schnaper H W. SP1 and Smad proteins cooperate to mediate transforming growth factor-beta 1-induced alpha 2(I) collagen expression in human glomerular mesangial cells. J Biol Chem, 2001, 276: 6983-6992
[23]  23 Sysa P, Potter J J, Liu X, et al. Transforming growth factor-beta1 up-regulation of human alpha(1)(I) collagen is mediated by SP1 and Smad2 transacting factors. DNA Cell Biol, 2009, 28: 425-434

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