Abstract:MicroRNAs (miRNAs) are a class of small non-coding RNAs, which mainly regulate gene expression through post-transcriptional process. They are highly conserved, tissue-specific and highly specific in miRNA-binding on 3’-untranslated regions. MicroRNAs have been identified as crucial regulators in myocardial cell proliferation, differentiation and apoptosis, migration of cardiac neural crest cells, cardiac morphogenesis and cardiac patterning processes, which may provide a new insight into the research on developmental mechanism of congenital heart diseases. The research on miRNAs in congenital heart diseases includes clinical research and animal experiments. This article reviews two types of research advances, the mechanism of congenital heart diseases, and the current status and limitation of the domestic reports.
Yates LA, Norbury CJ, Gilbert RJ. The long and short ofmicroRNA[J]. Cell, 2013, 153(3): 516-519.
[5]
Ikeda S, Kong SW, Lu J, et al. Altered microRNA expression inhuman heart disease[J]. Physiol Genomics, 2007, 31(3): 367-373.
[6]
Kumarswamy R, Thum T. Non-coding RNAs in cardiac remodeling and heart failure[J]. Circ Res, 2013, 113(6): 676-689.
[7]
Kim GH. MicroRNA regulation of cardiac conduction andarrhythmias[J]. Transl Res, 2013, 161(5): 381-392.
[8]
Pan W, Zhong Y, Cheng C, et al. MiR-30-regulated autophagymediates angiotensin II-induced myocardial hypertrophy[J].PLoS One, 2013, 8(1): e53950.
[9]
Zhao Y, Ransom JF, Li A, et al. Dysregulation of cardiogenesis,cardiac conduction, and cell cycle in mice lacking miRNA-1-2[J]. Cell, 2007, 129(2): 303-317.
[10]
Boettger T, Braun T. A new level of complexity: the role ofmicroRNAs in cardiovascular development[J]. Circ Res, 2012,110(7): 1000-1013.
[11]
Zeng Y, Yi R, Cullen BR. Recognition and cleavage of primarymicroRNA precursors by the nuclear processing enzymeDrosha[J]. EMBO J, 2005, 24(1): 138-148.
[12]
Faller M, Toso D, Matsunaga M, et al. DGCR8 recognizesprimary transcripts of microRNAs through highly cooperativebinding and formation of higher-order structures[J]. RNA, 2010,16(8): 1570-1583.
[13]
Barr I, Smith AT, Senturia R, et al. DiGeorge critical region 8(DGCR8) is a double-cysteine-ligated heme protein[J]. J BiolChem, 2011, 286(19): 16716-16725.
[14]
Chakravarthy S, Sternberg SH, Kellenberger CA, et al.Substrate-specific kinetics of dicer-catalyzed RNA processing[J].J Mol Biol, 2010, 404(3): 392-402.
[15]
Haase AD, Jaskiewicz L, Zhang HD, et al. TRBP, a regulator ofcellular PKR and HIV-1 virus expression, interacts with Dicerand functions in RNA silencing[J]. EMBO Rep, 2005, 6(10):961-967.
[16]
Chen J, Wang DZ. microRNAs in cardiovasculardevelopment[J]. J Mol Cell Cardiol, 2012, 52(5): 949-957.
[17]
Huang ZP, Chen JF, Regan JN, et al. Loss of microRNAs inneural crest leads to cardiovascular syndromes resemblinghuman congenital heart defects[J]. Arterioscler Thromb VascBiol, 2010, 30(12): 2575-2586.
[18]
Ambros V. The functions of animal microRNAs[J]. Nature,2004, 431(7006): 350-355.
[19]
Hashimoto Y, Akiyama Y, Yuasa Y. Multiple-to-multiplerelationships between microRNAs and target genes in gastriccancer[J]. PLoS One, 2013, 8(5): e62589.
[20]
Liu N, Olson EN. MicroRNA regulatory networks incardiovascular development[J]. Dev Cell, 2010, 18(4): 510-525.
[21]
Chen JF, Mandel EM, Thomson JM, et al. The role ofmicroRNA-1 and microRNA-133 in skeletal muscle proliferationand differentiation[J]. Nat Genet, 2006, 38(2): 228-233.
[22]
Li J, Cao Y, Ma XJ, et al. Roles of miR-1-1 and miR-181c inventricular septal defects[J]. Int J Cardiol, 2013, 168(2): 1441-1446.
[23]
Akiyama H, Chaboissier MC, Behringer RR, et al. Essential roleof Sox9 in the pathway that controls formation of cardiac valvesand septa[J]. Proc Natl Acad Sci U S A, 2004, 101(17): 6502-6507.
[24]
Sanchez-Castro M, Gordon CT, Petit F, et al. Congenital heartdefects in patients with deletions upstream of SOX9[J]. HumMutat, 2013, 34(12): 1628-1631.
[25]
Yang B, Lin H, Xiao J, et al. The muscle-specific microRNAmiR-1 regulates cardiac arrhythmogenic potential by targetingGJA1 and KCNJ2[J]. Nat Med, 2007, 13(4): 486-491.
[26]
Beppu H, Malhotra R, Beppu Y, et al. BMP type II receptorregulates positioning of outflow tract and remodeling ofatrioventricular cushion during cardiogenesis[J]. Dev Biol,2009, 331(2): 167-175.
[27]
Ma LJ, Lu MF, Schwartz RJ, et al. Bmp2 is essential for cardiaccushion epithelial-mesenchymal transition and myocardialpatterning[J]. Development, 2005, 132(24): 5601-5611.
[28]
O'Brien JE Jr, Kibiryeva N, Zhou XG, et al. Noncoding RNAexpression in myocardium from infants with tetralogy ofFallot[J]. Circ Cardiovasc Genet, 2012, 5(3): 279-286.
[29]
Chinchilla A, Lozano E, Daimi H, et al. MicroRNA profilingduring mouse ventricular maturation: a role for miR-27modulating Mef2c expression[J]. Cardiovasc Res, 2011, 89(1):98-108.
[30]
Wang J, Song Y, Zhang Y, et al. Cardiomyocyte overexpressionof miR-27b induces cardiac hypertrophy and dysfunction inmice[J]. Cell Res, 2012, 22(3): 516-527.
[31]
Huang X, Huang F, Yang D, et al. Expression of microRNA-122contributes to apoptosis in H9C2 myocytes[J]. J Cell Mol Med,2012, 16(11): 2637-2646.
[32]
Zhang HS, Wu QY, Xu M, et al. Mitogen-activated proteinkinase signal pathways play an important role in right ventricularhypertrophy of tetralogy of Fallot[J]. Chin Med J (Engl), 2012,125(13): 2243-2249.
Brown RD, Ambler SK, Li M, et al. MAP kinase kinasekinase-2 (MEKK2) regulates hypertrophic remodeling of theright ventricle in hypoxia-induced pulmonary hypertension[J].Am J Physiol Heart Circ Physiol, 2013, 304(2): H269-H281.
[35]
Nigam V, Sievers HH, Jensen BC, et al. Altered microRNAsin bicuspid aortic valve: a comparison between stenotic andinsufficient valves[J]. J Heart Valve Dis, 2010, 19(4): 459-465.
[36]
Kaden JJ, Bickelhaupt S, Grobholz R, et al. Expression of bonesialoprotein and bone morphogenetic protein-2 in calcific aorticstenosis[J]. J Heart Valve Dis, 2004, 13(4): 560-566.
[37]
Yu ZB, Han SP, Bai YF, et al. microRNA expression profilingin fetal single ventricle malformation identified by deepsequencing[J]. Int J Mol Med, 2012, 29(1): 53-60.
[38]
Liu YG, Huang TW, Zhao XL, et al. MicroRNAs modulatethe Wnt signaling pathway through targeting its inhibitors[J].Biochem Biophys Res Commun, 2011, 408(2): 259-264.
[39]
Kuhn DE, Nuovo GJ, Martin MM, et al. Human chromosome21-derived miRNAs are overexpressed in down syndrome brainsand hearts[J]. Biochem Biophys Res Commun, 2008, 370(3):473-477.
[40]
Liu N, Bezprozvannaya S, Williams AH, et al. microRNA-133aregulates cardiomyocyte proliferation and suppresses smoothmuscle gene expression in the heart[J]. Genes Dev, 2008,22(23): 3242-3254.
[41]
Nagy A. Cre recombinase: the universal reagent for genometailoring[J]. Genesis, 2000, 26(2): 99-109.