scholarly journals Cardiac gene expression profiling may reveal key differences between physiologic and pathologic cardiac hypertrophy

2005 ◽  
Vol 185 (4) ◽  
pp. 257-257
Author(s):  
Maurice H. Laughlin
Keyword(s):  
Gene Expression ◽  
Cardiac Hypertrophy ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Cardiac Gene Expression ◽  
Cardiac Gene ◽  
Pathologic Cardiac Hypertrophy

Abstract 751: Integrated Genetic Linkage Analysis and Expression Profiling in the Rat Heart to Identify Primary Drivers of Cardiac Hypertrophy

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Rizwan Sarwar ◽  
Enrico Petretto ◽  
Han Lu ◽  
Blanche Schroen ◽  
Mande K Kumaran ◽  
...  
Keyword(s):  
Gene Expression ◽  
Linkage Analysis ◽  
Cardiac Hypertrophy ◽  
Expression Profiling ◽  
Genetic Linkage ◽  
Genetic Linkage Analysis ◽  
Cardiac Gene Expression ◽  
Genome Wide ◽  
Cardiac Gene ◽  
Rat Genome

Intro: Although up to 60% of left ventricular mass (LVM) can be accounted for by extra-cardiac factors, the cause of remaining variance is uncharacterised. Hypothesis: Cardiac gene expression is under genetic control and these genetic effects account, at least in part, for the uncharacterised component of LVM. Method: We combined genetic linkage analysis with genome-wide expression profiling in a recombinant inbred (RI) rat strain panel to map the genetic determinants of cardiac gene expression, taking into account naturally occurring variation in blood pressure. Cardiac gene expression in 29 RI strains was quantified with 128 Affymetrix 230 2.0 microarrays, and linkage analysis of gene expression was performed with correction for multiple testing. Candidate genes for LVM were defined as gene colocalised with regions of the rat genome previously associated with LVM. Candidate genes identified in the rat were prioritised by assessing whether their human orthologues were dynamically regulated in heart biopsies from patients with cardiac hypertrophy undergoing surgery for aortic stenosis ( n =20) as compared to controls ( n =7), as determined with Affymetrix U133 microarrays. Results: We showed that genetic regulation of cardiac transcription is predominant when compared to extra-cardiac effects. This enabled us to determine the major control points of cardiac gene expression in the rat ( n =3,744, genome-wide P <0.05). A subset of 50 genes that mapped to themselves and colocalised with regions of the rat genome known to regulate LVM were identified. One of these 50 rat genes was mimecan or osteoglycin precursor ( Ogn ), whose orthologue showed the highest correlation with LVM out of the 22,284 probesets used in the human microarray analysis ( r =0.62, P =0.0008). We went on to refine the rat QTL associated with Ogn (peak LOD 4), and identified sequence variations that might be causative. We then showed that cardiac protein levels of OGN are increased in both rat and human hypertrophy. Conc: Combined linkage and expression studies provide a new and powerful systems approach to dissecting the pathophysiology of genetically complex traits. These data implicate Ogn as a primary genetic driver and biomarker of cardiac hypertrophy and warrant further functional testing.

Fish and chips: Cardiac gene expression profiling in the anoxia tolerant epaulette shark

2006 ◽  
Vol 41 (4) ◽  
pp. 733-733
Author(s):  
Kevin J. Ashton ◽  
Grant Pritchard ◽  
Gillian M.C. Renshaw ◽  
John P. Headrick
Keyword(s):  
Gene Expression ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Epaulette Shark ◽  
Cardiac Gene Expression ◽  
Cardiac Gene

scholarly journals Cardiac Gene Expression Profiling Provides Evidence for Cytokinopathy as a Molecular Mechanism in Chagas' Disease Cardiomyopathy

2005 ◽  
Vol 167 (2) ◽  
pp. 305-313 ◽  
Author(s):  
Edecio Cunha-Neto ◽  
Victor J. Dzau ◽  
Paul D. Allen ◽  
Dimitri Stamatiou ◽  
Luiz Benvenutti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profiling ◽  
Molecular Mechanism ◽  
Chagas Disease ◽  
Expression Profiling ◽  
Cardiac Gene Expression ◽  
Cardiac Gene

scholarly journals Cardiac gene expression profiling – the quest for an atrium-specific biomarker

2010 ◽  
Vol 18 (12) ◽  
pp. 610-614 ◽  
Author(s):  
A.H. Maass ◽  
A-M.R. De Jong ◽  
J. Frederiks ◽  
M.D. Smit ◽  
L. Gouweleeuw ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Cardiac Gene Expression ◽  
Cardiac Gene

Myoglobin-deficient mice activate a distinct cardiac gene expression program in response to isoproterenol-induced hypertrophy

2010 ◽  
Vol 41 (2) ◽  
pp. 137-145 ◽  
Author(s):  
Andrei Molojavyi ◽  
Antje Lindecke ◽  
Annika Raupach ◽  
Sarah Moellendorf ◽  
Karl Köhrer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cardiac Hypertrophy ◽  
Left Ventricular ◽  
Gene Expression Program ◽  
Cardiac Stress ◽  
Cardiac Gene Expression ◽  
Left Ventricular Dilatation ◽  
Cardiac Gene ◽  
Expression Program ◽  
Deficient Mice

Myoglobin knockout mice (myo−/−) adapt to the loss of myoglobin by the activation of a variety of compensatory mechanisms acting on the structural and functional level. To analyze to what extent myo−/− mice would tolerate cardiac stress we used the model of chronic isoproterenol application to induce cardiac hypertrophy in myo−/− mice and wild-type (WT) controls. After 14 days of isoproterenol infusion cardiac hypertrophy in WT and myo−/− mice reached a similar level. WT mice developed lung edema and left ventricular dilatation suggesting the development of heart failure. In contrast, myo−/− mice displayed conserved cardiac function and no signs of left ventricular dilatation. Analysis of the cardiac gene expression profiles using 40K mouse oligonucleotide arrays showed that isoproterenol affected the expression of 180 genes in WT but only 92 genes of myo−/− hearts. Only 40 of these genes were regulated in WT as well as in myo−/− hearts. In WT hearts a pronounced induction of genes of the extracellular matrix occurred suggesting a higher level of cardiac remodeling. myo−/− hearts showed altered transcription of genes involved in carbon metabolism, inhibition of apoptosis and muscular repair. Interestingly, a subset of genes that was altered in myo−/− mice already under basal conditions was differentially expressed in WT hearts under isoproterenol treatment. In summary, our data show a high capacity of myoglobin-deficient mice to adapt to catecholamine induced cardiac stress which is associated with activation of a distinct cardiac gene expression program.

Epigenetic control of exercise training-induced cardiac hypertrophy by miR-208

2016 ◽  
Vol 130 (22) ◽  
pp. 2005-2015 ◽  
Author(s):  
Ursula Paula Renó Soci ◽  
Tiago Fernandes ◽  
Valerio Garrone Barauna ◽  
Nara Yumi Hashimoto ◽  
Gloria de Fátima Alves Mota ◽  
...  
Keyword(s):  
Gene Expression ◽  
Exercise Training ◽  
Cardiac Hypertrophy ◽  
Target Genes ◽  
Aerobic Training ◽  
Therapeutic Potential ◽  
Down Regulation ◽  
Epigenetic Control ◽  
Cardiac Gene Expression ◽  
Cardiac Gene

The physiological training-induced cardiac hypertrophy is epigenetically orchestrated by up-regulation of miR-208a/miR-208b and down-regulation of their target genes: Sox6, Med13, Purβ, SP3 and HP1β. These results highlight the therapeutic potential of aerobic training and miR-208 in cardiac gene expression.

Sign in / Sign up

Export Citation Format

Share Document