Myosin light chain composition in non-failing donor and end-stage failing human ventricular myocardium.

Abstract:

:The increased Ca(2+)-responsiveness in end-stage human heart failure cannot be attributed to contractile protein isoform changes, but rather is the complex resultant of changes in degree of phosphorylation of VLC-2 and TnI. Despite the decreased basal level of VLC-2 phosphorylation the response to VLC-2 dephosphorylation is enhanced in failing myocytes, which might result from differences in endogenous phosphorylation of thin and thick filament proteins between donor and failing hearts. Taken together decreased VLC-2 phosphorylation in end-stage human heart failure might represent a compensatory process leading to an improvement of myocardial contractility by opposing the detrimental effects of increased Ca(2+)-responsiveness of force and impaired Ca(2+)-handling on diastolic function.

journal_name

Adv Exp Med Biol

authors

van der Velden J,Papp Z,Boontje NM,Zaremba R,de Jong JW,Janssen PM,Hasenfuss G,Stienen GJ

doi

10.1007/978-1-4419-9029-7_1

subject

Has Abstract

pub_date

2003-01-01 00:00:00

pages

3-15

eissn

0065-2598

issn

2214-8019

journal_volume

538

pub_type

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