Literature DB >> 14984723

Left-right asymmetric ventricular expression of CARP in the piglet heart: regional response to experimental heart failure.

Mario Torrado1, Eduardo López, Alberto Centeno, Alfonso Castro-Beiras, Alexander T Mikhailov.   

Abstract

BACKGROUND AND AIM: Cardiac ankyrin repeat protein (CARP), whose expression is down-regulated in response to doxorubicin (Dox) in vitro, has been proposed to be a marker of experimentally-induced cardiac hypertrophy in rodent models. In piglets, the rapid hypertrophy rate of the left ventricle (LV) as compared to that of the right ventricle (RV) represents a natural model of asymmetric ventricular enlargement. We tested whether CARP expression correlates with postnatal ventricular hypertrophy and to what extent CARP can be sensitive to Dox treatment in vivo.
METHODS: CARP mRNA and protein levels were quantified (by Northern blot hybridization, semi-quantitative RT-PCR and Western blot) in the piglet heart, both during early postnatal development and upon Dox-induced cardiomyopathy (Dox-CM).
RESULTS: The study revealed: (1) significantly augmented CARP mRNA and protein levels in the LV compared to the RV resulting in left vs. right asymmetry in ventricular CARP expression throughout early postnatal development; (2) dose- and chamber-dependent CARP mRNA and protein enrichment in ventricular myocardium in response to Dox; and (3) abolishment of asymmetric patterns of ventricular CARP expression at heart failure resulting from Dox-CM.
CONCLUSIONS: (1) CARP is differentially regulated in the LV and RV during both postnatal development and disease; and (2) monitoring of ventricular CARP expression patterns can be used for further analysis of transition from compensated to overt heart failure.

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Year:  2004        PMID: 14984723     DOI: 10.1016/j.ejheart.2003.11.004

Source DB:  PubMed          Journal:  Eur J Heart Fail        ISSN: 1388-9842            Impact factor:   15.534


  14 in total

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Review 4.  Mechanotransduction in cardiac hypertrophy and failure.

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Review 5.  Understanding the molecular basis of cardiomyopathy.

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6.  ANKRD1, the gene encoding cardiac ankyrin repeat protein, is a novel dilated cardiomyopathy gene.

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7.  Identification of candidate genes potentially relevant to chamber-specific remodeling in postnatal ventricular myocardium.

Authors:  Mario Torrado; Raquel Iglesias; Beatriz Nespereira; Alexander T Mikhailov
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8.  Overexpression of CYP2J2 provides protection against doxorubicin-induced cardiotoxicity.

Authors:  Yunfang Zhang; Haitham El-Sikhry; Ketul R Chaudhary; Sri Nagarjun Batchu; Anooshirvan Shayeganpour; Taibeh Orujy Jukar; J Alyce Bradbury; Joan P Graves; Laura M DeGraff; Page Myers; Douglas C Rouse; Julie Foley; Abraham Nyska; Darryl C Zeldin; John M Seubert
Journal:  Am J Physiol Heart Circ Physiol       Date:  2009-05-08       Impact factor: 4.733

9.  In search of novel targets for heart disease: myocardin and myocardin-related transcriptional cofactors.

Authors:  Alexander T Mikhailov; Mario Torrado
Journal:  Biochem Res Int       Date:  2012-05-17

10.  Cardiac ankyrin repeat protein attenuates cardiac hypertrophy by inhibition of ERK1/2 and TGF-β signaling pathways.

Authors:  Yao Song; Jialin Xu; Yanfeng Li; Chunshi Jia; Xiaowei Ma; Lei Zhang; Xiaojie Xie; Yong Zhang; Xiang Gao; Youyi Zhang; Dahai Zhu
Journal:  PLoS One       Date:  2012-12-05       Impact factor: 3.240

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