Adverse Intrauterine Environment and Cardiac miRNA Expression

被引:22
作者
Lock, Mitchell C. [1 ]
Botting, Kimberley J. [1 ]
Tellam, Ross L. [1 ,2 ]
Brooks, Doug [3 ]
Morrison, Janna L. [1 ]
机构
[1] Univ South Australia, Early Origins Adult Hlth Res Grp, Sch Pharm & Med Sci, Sansom Inst Hlth Res, Adelaide, SA 5001, Australia
[2] CSIRO Agr, 306 Carmody Rd, St Lucia, Qld 4067, Australia
[3] Univ South Australia, Mech Cell Biol & Dis Res Grp, Sch Pharm & Med Sci, Sansom Inst Hlth Res, Adelaide, SA 5001, Australia
基金
澳大利亚国家健康与医学研究理事会;
关键词
miRNA; epigenetics; heart disease; fetal development; CORONARY-HEART-DISEASE; MICRORNA EXPRESSION; GROWTH RESTRICTION; PRENATAL HYPOXIA; HIGH-ALTITUDE; FETAL-GROWTH; CELL-CYCLE; UTEROPLACENTAL INSUFFICIENCY; THERAPEUTIC INHIBITION; DILATED CARDIOMYOPATHY;
D O I
10.3390/ijms18122628
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Placental insufficiency, high altitude pregnancies, maternal obesity/diabetes, maternal undernutrition and stress can result in a poor setting for growth of the developing fetus. These adverse intrauterine environments result in physiological changes to the developing heart that impact how the heart will function in postnatal life. The intrauterine environment plays a key role in the complex interplay between genes and the epigenetic mechanisms that regulate their expression. In this review we describe how an adverse intrauterine environment can influence the expression of miRNAs (a sub-set of non-coding RNAs) and how these changes may impact heart development. Potential consequences of altered miRNA expression in the fetal heart include; Hypoxia inducible factor (HIF) activation, dysregulation of angiogenesis, mitochondrial abnormalities and altered glucose and fatty acid transport/metabolism. It is important to understand how miRNAs are altered in these adverse environments to identify key pathways that can be targeted using miRNA mimics or inhibitors to condition an improved developmental response.
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页数:19
相关论文
共 145 条
[91]   Cardiac-specific deletion of Gata4 reveals its requirement for hypertrophy, compensation, and myocyte viability [J].
Oka, T ;
Maillet, M ;
Watt, AJ ;
Schwartz, RJ ;
Aronow, BJ ;
Duncan, SA ;
Molkentin, JD .
CIRCULATION RESEARCH, 2006, 98 (06) :837-845
[92]   Mitochondrial morphology and cardiovascular disease [J].
Ong, Sang-Bing ;
Hausenloy, Derek J. .
CARDIOVASCULAR RESEARCH, 2010, 88 (01) :16-29
[93]   Review: Placenta-specific microRNAs in exosomes Good things come in nano-packages [J].
Ouyang, Y. ;
Mouillet, J. -F. ;
Coyne, C. B. ;
Sadovsky, Y. .
PLACENTA, 2014, 35 :S69-S73
[94]   miR-146a targets Fos expression in human cardiac cells [J].
Palomer, Xavier ;
Capdevila-Busquets, Eva ;
Botteri, Gaia ;
Davidson, Mercy M. ;
Rodriguez, Cristina ;
Martinez-Gonzalez, Jose ;
Vidal, Francisco ;
Barroso, Emma ;
Chan, Tung O. ;
Feldman, Arthur M. ;
Vazquez-Carrera, Manuel .
DISEASE MODELS & MECHANISMS, 2015, 8 (09) :1081-1091
[95]   Phosphorylation-activity relationships of AMPK and acetyl-CoA carboxylase in muscle [J].
Park, SH ;
Gammon, SR ;
Knippers, JD ;
Paulsen, SR ;
Rubink, DS ;
Winder, WW .
JOURNAL OF APPLIED PHYSIOLOGY, 2002, 92 (06) :2475-2482
[96]  
Patterson AJ, 2010, CURR MOL MED, V10, P653
[97]   Chronic Prenatal Hypoxia Induces Epigenetic Programming of PKCε Gene Repression in Rat Hearts [J].
Patterson, Andrew J. ;
Chen, Man ;
Xue, Qin ;
Xiao, Daliao ;
Zhang, Lubo .
CIRCULATION RESEARCH, 2010, 107 (03) :365-373
[98]   Prenatal environmental exposures, epigenetics, and disease [J].
Perera, Frederica ;
Herbstman, Julie .
REPRODUCTIVE TOXICOLOGY, 2011, 31 (03) :363-373
[99]   Role of microRNAs in allergic asthma: present and future [J].
Perry, Mark M. ;
Adcock, Ian M. ;
Chung, Kian Fan .
CURRENT OPINION IN ALLERGY AND CLINICAL IMMUNOLOGY, 2015, 15 (02) :156-162
[100]   External influences on the fetus and their long-term consequences [J].
Phillips, D. I. W. .
LUPUS, 2006, 15 (11) :794-800