Literature DB >> 17157829

Differential distribution and regulation of mouse cardiac Na+/K+-ATPase alpha1 and alpha2 subunits in T-tubule and surface sarcolemmal membranes.

Roger G Berry1, Sanda Despa, William Fuller, Donald M Bers, Michael J Shattock.   

Abstract

OBJECTIVES: Two Na+/K+-ATPase (NKA) alpha-subunit isoforms, alpha1 and alpha2, are expressed in the adult mouse heart. The subcellular distribution of these isoforms in T-tubule and surface sarcolemmal (SSL) membranes and their regulation by cAMP-dependent protein kinase (PKA) is unclear.
METHODS: We used formamide-induced detubulation of mouse ventricular myocytes to investigate differential functional distribution and regulation by PKA of alpha1 and alpha2 in T-tubule versus SSL membranes by measuring NKA current (I(pump)) and NKA-mediated Na+ efflux (-d[Na](i)/dt).
RESULTS: I(pump) is composed of 88% alpha(1)-mediated I(pump) (Ialpha1) and 12% alpha2-mediated I(pump) (Ialpha2). alpha1 and alpha2 subunits demonstrate distinct ouabain affinities (105+/-6 and 0.3+/-0.1 micromol/L respectively) but similar affinity for intracellular Na+ (K(1/2)Na+ of 16.6+/-0.8 and 16.7+/-2.6 mmol/L respectively). Detubulation reduced (i) I(pump) density (1.42+/-0.1 to 1.20+/-0.04 pA/pF), (ii) cell capacitance (181+/-12 to 127+/-17 pF), and (iii) Ialpha2 contribution (12 to 6%). Total I(pump) density was approximately 60% higher in T-tubule (1.94 pA/pF, derived) vs. SSL membranes. Although T-tubule membranes represent only 30% of total surface area, they generate approximately 70% of Ialpha2 and approximately 37% of Ialpha1. Ialpha1 density was substantially higher than Ialpha2 in SSL (Ialpha1:Ialpha2 = 16:1) but this was markedly reduced in T-tubules (4:1). In addition to differential localisation, isoprenaline (ISO, 1 micromol/L) significantly increased alpha1-mediated NKA Na+ affinity (from 16.6+/-0.8 to 13.3+/-1.4 mmol/L) and caused a small increase in maximal NKA Na+ efflux rate. ISO had no effect on alpha2-mediated NKA activity.
CONCLUSION: These data suggest that NKA alpha1 and alpha2 subunits are differentially localised and regulated by PKA in T-tubule and SSL membranes and may have distinct regulatory roles in cardiac excitation-contraction coupling.

Entities:  

Mesh:

Substances:

Year:  2006        PMID: 17157829     DOI: 10.1016/j.cardiores.2006.11.006

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


  51 in total

1.  Ankyrin-B reduction enhances Ca spark-mediated SR Ca release promoting cardiac myocyte arrhythmic activity.

Authors:  Emmanuel Camors; Peter J Mohler; Donald M Bers; Sanda Despa
Journal:  J Mol Cell Cardiol       Date:  2012-03-03       Impact factor: 5.000

2.  Uniform action potential repolarization within the sarcolemma of in situ ventricular cardiomyocytes.

Authors:  Guixue Bu; Heather Adams; Edward J Berbari; Michael Rubart
Journal:  Biophys J       Date:  2009-03-18       Impact factor: 4.033

Review 3.  Pivotal role of α2 Na+ pumps and their high affinity ouabain binding site in cardiovascular health and disease.

Authors:  Mordecai P Blaustein; Ling Chen; John M Hamlyn; Frans H H Leenen; Jerry B Lingrel; W Gil Wier; Jin Zhang
Journal:  J Physiol       Date:  2016-07-31       Impact factor: 5.182

Review 4.  How does pressure overload cause cardiac hypertrophy and dysfunction? High-ouabain affinity cardiac Na+ pumps are crucial.

Authors:  Mordecai P Blaustein
Journal:  Am J Physiol Heart Circ Physiol       Date:  2017-07-21       Impact factor: 4.733

5.  The central role of protein kinase C epsilon in cyanide cardiotoxicity and its treatment.

Authors:  Joseph Y Cheung; Salim Merali; JuFang Wang; Xue-Qian Zhang; Jianliang Song; Carmen Merali; Dhanendra Tomar; Hanning You; Annick Judenherc-Haouzi; Philippe Haouzi
Journal:  Toxicol Sci       Date:  2019-06-07       Impact factor: 4.849

6.  Knockout of the Na,K-ATPase α2-isoform in cardiac myocytes delays pressure overload-induced cardiac dysfunction.

Authors:  Tara N Rindler; Valerie M Lasko; Michelle L Nieman; Motoi Okada; John N Lorenz; Jerry B Lingrel
Journal:  Am J Physiol Heart Circ Physiol       Date:  2013-02-22       Impact factor: 4.733

7.  Overexpression of the Na+/K+ ATPase α2 but not α1 isoform attenuates pathological cardiac hypertrophy and remodeling.

Authors:  Robert N Correll; Petra Eder; Adam R Burr; Sanda Despa; Jennifer Davis; Donald M Bers; Jeffery D Molkentin
Journal:  Circ Res       Date:  2013-11-11       Impact factor: 17.367

8.  Sodium accumulation promotes diastolic dysfunction in end-stage heart failure following Serca2 knockout.

Authors:  William E Louch; Karina Hougen; Halvor K Mørk; Fredrik Swift; Jan M Aronsen; Ivar Sjaastad; Henrik M Reims; Borghild Roald; Kristin B Andersson; Geir Christensen; Ole M Sejersted
Journal:  J Physiol       Date:  2009-12-14       Impact factor: 5.182

9.  Phospholemman and beta-adrenergic stimulation in the heart.

Authors:  JuFang Wang; Erhe Gao; Jianliang Song; Xue-Qian Zhang; Jifen Li; Walter J Koch; Amy L Tucker; Kenneth D Philipson; Tung O Chan; Arthur M Feldman; Joseph Y Cheung
Journal:  Am J Physiol Heart Circ Physiol       Date:  2009-12-11       Impact factor: 4.733

Review 10.  There goes the neighborhood: pathological alterations in T-tubule morphology and consequences for cardiomyocyte Ca2+ handling.

Authors:  William E Louch; Ole M Sejersted; Fredrik Swift
Journal:  J Biomed Biotechnol       Date:  2010-04-08
View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.