Literature DB >> 12504816

Combined phospholamban ablation and SERCA1a overexpression result in a new hyperdynamic cardiac state.

Wen Zhao1, Konrad F Frank, Guoxiang Chu, Michael J Gerst, Albrecht G Schmidt, Yong Ji, Muthu Periasamy, Evangelia G Kranias.   

Abstract

OBJECTIVE: Phospholamban ablation or ectopic expression of SERCA1a in the heart results in significant increases in cardiac contractile parameters. The aim of the present study was to determine whether a combination of these two genetic manipulations may lead to further augmentation of cardiac function.
METHODS: Transgenic mice with cardiac specific overexpression of SERCA1a were mated with phospholamban deficient mice to generate a model with SERCA1a overexpression in the phospholamban null background (SERCA1(OE)/PLB(KO)). The cardiac phenotype was characterized using quantitative immunoblotting, sarcoplasmic reticulum calcium uptake and single myocyte mechanics and calcium kinetics.
RESULTS: Quantitative immunoblotting revealed an increase of 1.8-fold in total SERCA level, while SERCA2 was decreased to 50% of wild types. Isolated myocytes indicated increases in the maximal rates of contraction by 195 and 125%, the maximal rates of relaxation by 200 and 124%, while the time for 80% decay of the Ca(2+)-transient was decreased to 43 and 75%, in SERCA1(OE)/PLB(KO) hearts, compared to SERCA1a overexpressors and phospholamban knockouts, respectively. These mechanical alterations reflected parallel alterations in V(max) and EC(50) for Ca(2+) of the sarcoplasmic reticulum Ca(2+) transport system. Furthermore, there were no significant cardiac histological or pathological alterations, and the myocyte contractile parameters remained enhanced, up to 12 months of age.
CONCLUSIONS: These findings suggest that a combination of SERCA1a overexpression and phospholamban ablation results in further enhancement of myocyte contractility over each individual alteration.

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Year:  2003        PMID: 12504816     DOI: 10.1016/s0008-6363(02)00609-0

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


  10 in total

1.  Contractility of ventricular myocytes is well preserved despite altered mechanisms of Ca2+ transport and a changing pattern of mRNA in aged type 2 Zucker diabetic fatty rat heart.

Authors:  F C Howarth; M A Qureshi; Z Hassan; D Isaev; K Parekh; A John; M Oz; H Raza; E Adeghate; T E Adrian
Journal:  Mol Cell Biochem       Date:  2011-10-19       Impact factor: 3.396

2.  Phospholamban phosphorylation, mutation, and structural dynamics: a biophysical approach to understanding and treating cardiomyopathy.

Authors:  Naa-Adjeley D Ablorh; David D Thomas
Journal:  Biophys Rev       Date:  2015-01-21

3.  Intra-sarcoplasmic reticulum Ca2+ oscillations are driven by dynamic regulation of ryanodine receptor function by luminal Ca2+ in cardiomyocytes.

Authors:  Sarah C W Stevens; Dmitry Terentyev; Anuradha Kalyanasundaram; Muthu Periasamy; Sandor Györke
Journal:  J Physiol       Date:  2009-08-24       Impact factor: 5.182

4.  Decreased RyR2 refractoriness determines myocardial synchronization of aberrant Ca2+ release in a genetic model of arrhythmia.

Authors:  Lucia Brunello; Jessica L Slabaugh; Przemyslaw B Radwanski; Hsiang-Ting Ho; Andriy E Belevych; Qing Lou; Haiyan Chen; Carlo Napolitano; Francesco Lodola; Silvia G Priori; Vadim V Fedorov; Pompeo Volpe; Michael Fill; Paul M L Janssen; Sándor Györke
Journal:  Proc Natl Acad Sci U S A       Date:  2013-06-03       Impact factor: 11.205

5.  A mutation in calsequestrin, CASQ2D307H, impairs Sarcoplasmic Reticulum Ca2+ handling and causes complex ventricular arrhythmias in mice.

Authors:  Wessel P Dirksen; Veronique A Lacombe; Mei Chi; Anuradha Kalyanasundaram; Serge Viatchenko-Karpinski; Dmitry Terentyev; Zhixiang Zhou; Srikanth Vedamoorthyrao; Ning Li; Nipavan Chiamvimonvat; Cynthia A Carnes; Clara Franzini-Armstrong; Sandor Györke; Muthu Periasamy
Journal:  Cardiovasc Res       Date:  2007-03-12       Impact factor: 10.787

6.  Rescue of cardiomyocyte dysfunction by phospholamban ablation does not prevent ventricular failure in genetic hypertrophy.

Authors:  Qiujing Song; Albrecht G Schmidt; Harvey S Hahn; Andrew N Carr; Beate Frank; Luke Pater; Mike Gerst; Karen Young; Brian D Hoit; Bradley K McConnell; Kobra Haghighi; Christine E Seidman; Jonathan G Seidman; Gerald W Dorn; Evangelia G Kranias
Journal:  J Clin Invest       Date:  2003-03       Impact factor: 14.808

7.  Synthetic phosphopeptides enable quantitation of the content and function of the four phosphorylation states of phospholamban in cardiac muscle.

Authors:  Naa-Adjeley D Ablorh; Xiaoqiong Dong; Zachary M James; Qiang Xiong; Jianyi Zhang; David D Thomas; Christine B Karim
Journal:  J Biol Chem       Date:  2014-09-04       Impact factor: 5.157

8.  Up-regulation of sarcoplasmic reticulum Ca(2+) uptake leads to cardiac hypertrophy, contractile dysfunction and early mortality in mice deficient in CASQ2.

Authors:  Anuradha Kalyanasundaram; Véronique A Lacombe; Andriy E Belevych; Lucia Brunello; Cynthia A Carnes; Paul M L Janssen; Bjørn C Knollmann; Muthu Periasamy; Sandor Gyørke
Journal:  Cardiovasc Res       Date:  2012-11-06       Impact factor: 10.787

9.  Exposure to N-ethyl-N-nitrosourea in adult mice alters structural and functional integrity of neurogenic sites.

Authors:  Vivian Capilla-Gonzalez; Sara Gil-Perotin; Antonio Ferragud; Luis Bonet-Ponce; Juan Jose Canales; Jose Manuel Garcia-Verdugo
Journal:  PLoS One       Date:  2012-01-04       Impact factor: 3.240

Review 10.  Mitochondrial and Sarcoplasmic Reticulum Interconnection in Cardiac Arrhythmia.

Authors:  Felipe Salazar-Ramírez; Roberto Ramos-Mondragón; Gerardo García-Rivas
Journal:  Front Cell Dev Biol       Date:  2021-01-28
  10 in total

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