Literature DB >> 12619861

Compensated hypertrophy of cardiac ventricles in aged transgenic FVB/N mice overexpressing calsequestrin.

Yoji Sato1, Albrecht G Schmidt, Helen Kiriazis, Brian D Hoit, Evangelia G Kranias.   

Abstract

Cardiac-specific overexpression of murine cardiac calsequestrin results in depressed contractile parameters and hypertrophy in transgenic mice. To determine the long-term consequences of calsequestrin overexpression, the cardiac phenotype of young (2-3-months old) and aged (17 months old) transgenic FVB/N mice was characterized. Ventricular/body weight ratios, which were increased in young transgenics compared with wild-types, were unaltered with age. Left atria of aged transgenics exhibited enlargement and mineralization, but their ventricles did not display fibrosis, mineralization and other injuries. Although echocardiography suggested a time-dependent change in ventricular geometry and loading conditions in vivo, as well as an age-dependent reduction of left ventricular fractional shortening in transgenic mice, Langendorff-perfused hearts of young and aged transgenics indicated that there were no age-related reductions of contractile parameters (+/-dP/dt). Furthermore, neither genotype nor age altered lung/body weight ratios. Thus, our findings suggest that left ventricular performance in calsequestrin overexpressing mice becomes apparently depressed with age, but this depression is not associated with progressive reduction of left ventricular contractility and heart failure.

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Year:  2003        PMID: 12619861

Source DB:  PubMed          Journal:  Mol Cell Biochem        ISSN: 0300-8177            Impact factor:   3.396


  21 in total

1.  Remodelling of ionic currents in hypertrophied and failing hearts of transgenic mice overexpressing calsequestrin.

Authors:  B C Knollmann; B E Knollmann-Ritschel; N J Weissman; L R Jones; M Morad
Journal:  J Physiol       Date:  2000-06-01       Impact factor: 5.182

2.  Complex formation between junctin, triadin, calsequestrin, and the ryanodine receptor. Proteins of the cardiac junctional sarcoplasmic reticulum membrane.

Authors:  L Zhang; J Kelley; G Schmeisser; Y M Kobayashi; L R Jones
Journal:  J Biol Chem       Date:  1997-09-12       Impact factor: 5.157

3.  Contractile reserve and intracellular calcium regulation in mouse myocytes from normal and hypertrophied failing hearts.

Authors:  K Ito; X Yan; M Tajima; Z Su; W H Barry; B H Lorell
Journal:  Circ Res       Date:  2000-09-29       Impact factor: 17.367

4.  Cardiac-specific overexpression of calsequestrin results in left ventricular hypertrophy, depressed force-frequency relation and pulsus alternans in vivo.

Authors:  A G Schmidt; V J Kadambi; N Ball; Y Sato; R A Walsh; E G Kranias; B D Hoit
Journal:  J Mol Cell Cardiol       Date:  2000-09       Impact factor: 5.000

5.  Alterations of sarcoplasmic reticulum proteins in failing human dilated cardiomyopathy.

Authors:  M Meyer; W Schillinger; B Pieske; C Holubarsch; C Heilmann; H Posival; G Kuwajima; K Mikoshiba; H Just; G Hasenfuss
Journal:  Circulation       Date:  1995-08-15       Impact factor: 29.690

6.  Genetic analysis of dystrophic cardiac calcification in DBA/2 mice.

Authors:  F A van den Broek; R Bakker; M den Bieman; A X Fielmich-Bouwman; A G Lemmens; H A van Lith; I Nissen; J M Ritskes-Hoitinga; G van Tintelen; L F van Zutphen
Journal:  Biochem Biophys Res Commun       Date:  1998-12-18       Impact factor: 3.575

7.  Dystrophic cardiac calcinosis in mice: genetic, hormonal, and dietary influences.

Authors:  G J Eaton; R P Custer; F N Johnson; K T Stabenow
Journal:  Am J Pathol       Date:  1978-01       Impact factor: 4.307

8.  Left ventricular chamber dilatation in hypertrophic cardiomyopathy: related variables and prognosis in patients with medical and surgical therapy.

Authors:  C Seiler; R Jenni; G Vassalli; M Turina; O M Hess
Journal:  Br Heart J       Date:  1995-11

9.  Cardiac-specific overexpression of mouse cardiac calsequestrin is associated with depressed cardiovascular function and hypertrophy in transgenic mice.

Authors:  Y Sato; D G Ferguson; H Sako; G W Dorn; V J Kadambi; A Yatani; B D Hoit; R A Walsh; E G Kranias
Journal:  J Biol Chem       Date:  1998-10-23       Impact factor: 5.157

10.  Interaction of triadin with histidine-rich Ca(2+)-binding protein at the triadic junction in skeletal muscle fibers.

Authors:  R Sacchetto; F Turcato; E Damiani; A Margreth
Journal:  J Muscle Res Cell Motil       Date:  1999-05       Impact factor: 2.698

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  3 in total

1.  Cardiomyopathy of aging in the mammalian heart is characterized by myocardial hypertrophy, fibrosis and a predisposition towards cardiomyocyte apoptosis and autophagy.

Authors:  Andrew J Boyle; Henry Shih; Joy Hwang; Jianqin Ye; Brian Lee; Yan Zhang; David Kwon; Kristine Jun; Daiwei Zheng; Rich Sievers; Franca Angeli; Yerem Yeghiazarians; Randall Lee
Journal:  Exp Gerontol       Date:  2011-03-03       Impact factor: 4.032

2.  Normal cardiac function in mice with supraphysiological cardiac creatine levels.

Authors:  Lucia Santacruz; Alejandro Hernandez; Jeffrey Nienaber; Rajashree Mishra; Miguel Pinilla; James Burchette; Lan Mao; Howard A Rockman; Danny O Jacobs
Journal:  Am J Physiol Heart Circ Physiol       Date:  2013-11-22       Impact factor: 4.733

3.  Genetic background influences adaptation to cardiac hypertrophy and Ca(2+) handling gene expression.

Authors:  Steve B Waters; Douglass M Diak; Matthew Zuckermann; Paul H Goldspink; Lara Leoni; Brian B Roman
Journal:  Front Physiol       Date:  2013-03-06       Impact factor: 4.566

  3 in total

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