Effects of losartan on pressure overload-induced cardiac gene expression profiling in rats

2003 ◽  
Vol 30 (11) ◽  
pp. 827-832 ◽  
Author(s):  
Jinliang Li ◽  
Ping Li ◽  
Xinheng Feng ◽  
Zhaoping Li ◽  
Rong Hou ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Pressure Overload ◽  
Cardiac Gene Expression ◽  
Cardiac Gene

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

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.

scholarly journals Cardiac Pressure Overload Decreases ETV1 Expression in the Left Atrium, Contributing to Atrial Electrical and Structural Remodeling

Circulation ◽  
2020 ◽  
Author(s):  
Naoko Yamaguchi ◽  
Junhua Xiao ◽  
Deven Narke ◽  
Devin Shaheen ◽  
Xianming Lin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Gene Expression Profiling ◽  
Left Atrium ◽  
Expression Profiling ◽  
Left Atrial ◽  
Pressure Overload ◽  
Neonatal Rat ◽  
Rna Seq ◽  
Structural Remodeling

Background: Elevated intracardiac pressure due to heart failure induces electrical and structural remodeling in the left atrium (LA) that begets atrial myopathy and arrhythmias. The underlying molecular pathways that drive atrial remodeling during cardiac pressure overload are poorly defined. The purpose of this study is to characterize the response of the ETV1 signaling axis in the LA during cardiac pressure overload in humans and mouse models and explore the role of ETV1 in atrial electrical and structural remodeling. Methods: We performed gene expression profiling in 265 left atrial samples from patients who underwent cardiac surgery. Comparative gene expression profiling was performed between two murine models of cardiac pressure overload, transverse aortic constriction (TAC) banding and Angiotensin II (AngII) infusion, and a genetic model of Etv1 cardiomyocyte-selective knockout ( Etv1 f/f Mlc2a Cre/+ ). Results: Using the Cleveland Clinic biobank of human LA specimens, we found that ETV1 expression is decreased in patients with reduced ejection fraction. Consistent with its role as an important mediator of the Neuregulin-1 (NRG1) signaling pathway and activator of rapid conduction gene programming, we identified a direct correlation between ETV1 expression level and NRG1, ERBB4, SCN5A , and GJA5 levels in human LA samples. In a similar fashion to heart failure patients, we showed that left atrial ETV1 expression is downregulated at the RNA and protein levels in murine pressure overload models. Comparative analysis of LA RNA-seq datasets from TAC and AngII treated mice showed a high Pearson correlation, reflecting a highly ordered process by which the LA undergoes electrical and structural remodeling. Cardiac pressure overload produced a consistent downregulation of ErbB4, Etv1, Scn5a, and Gja5 and upregulation of profibrotic gene programming, which includes Tgfbr1/2, Igf1, and numerous collagen genes. Etv1 f/f Mlc2a Cre/+ mice displayed atrial conduction disease and arrhythmias. Correspondingly, the LA from Etv1 f/f Mlc2a Cre/+ mice showed downregulation of rapid conduction genes and upregulation of profibrotic gene programming, whereas analysis of a gain-of-function ETV1 RNA-seq dataset from neonatal rat ventricular myocytes transduced with Etv1 showed reciprocal changes. Conclusions: ETV1 is downregulated in the LA during cardiac pressure overload, contributing to both electrical and structural remodeling.

Sign in / Sign up

Export Citation Format

Share Document