Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis

Intracellular acidosis exerts substantial effects on the contractile performance of the heart. Soon after the onset of acidosis, contractility diminishes, largely due to a decrease in myofilament Ca2+ responsiveness. This decrease in contractility is followed by a progressive recovery that occurs de...

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Autores principales: Mattiazzi, Alicia Ramona, Vittone, Leticia, Mundiña-Weilenmann, Cecilia
Formato: Articulo Revision
Lenguaje:Inglés
Publicado: 2007
Materias:
Ciencias Médicas
Acidosis
CaMKII
Protein phosphorylation
SR function
Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/83199
Aporte de:
SEDICI (UNLP) de Universidad Nacional de La Plata
id I19-R120-10915-83199
record_format dspace
institution Universidad Nacional de La Plata
institution_str I-19
repository_str R-120
collection SEDICI (UNLP)
language Inglés
topic Ciencias Médicas
Acidosis
CaMKII
Protein phosphorylation
SR function
spellingShingle Ciencias Médicas
Acidosis
CaMKII
Protein phosphorylation
SR function
Mattiazzi, Alicia Ramona
Vittone, Leticia
Mundiña-Weilenmann, Cecilia
Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
topic_facet Ciencias Médicas
Acidosis
CaMKII
Protein phosphorylation
SR function
description Intracellular acidosis exerts substantial effects on the contractile performance of the heart. Soon after the onset of acidosis, contractility diminishes, largely due to a decrease in myofilament Ca2+ responsiveness. This decrease in contractility is followed by a progressive recovery that occurs despite the persistent acidosis. This recovery is the result of different mechanisms that converge to increase diastolic Ca2+ levels and Ca2+ transient amplitude. Recent experimental evidence indicates that activation of the Ca2+/calmodulin-dependent protein kinase II (CaMKII) is an essential step in the sequence of events that increases the Ca2+ transient amplitude and produces contractile recovery. CaMKII may act as an amplifier, providing compensatory pathways to offset the inhibitory effects of acidosis on many of the Ca2+ handling proteins. CaMKII-induced phosphorylation of the SERCA2a regulatory protein phospholamban (PLN) has the potential to promote an increase in sarcoplasmic reticulum (SR) Ca2+ uptake and SR Ca2+ load, and is a likely candidate to mediate the mechanical recovery from acidosis. In addition, CaMKII-dependent phosphorylation of proteins other than PLN may also contribute to this recovery.
format Articulo
Revision
author Mattiazzi, Alicia Ramona
Vittone, Leticia
Mundiña-Weilenmann, Cecilia
author_facet Mattiazzi, Alicia Ramona
Vittone, Leticia
Mundiña-Weilenmann, Cecilia
author_sort Mattiazzi, Alicia Ramona
title Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
title_short Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
title_full Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
title_fullStr Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
title_full_unstemmed Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
title_sort ca2+/calmodulin-dependent protein kinase: a key component in the contractile recovery from acidosis
publishDate 2007
url http://sedici.unlp.edu.ar/handle/10915/83199
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AT vittoneleticia ca2calmodulindependentproteinkinaseakeycomponentinthecontractilerecoveryfromacidosis
AT mundinaweilenmanncecilia ca2calmodulindependentproteinkinaseakeycomponentinthecontractilerecoveryfromacidosis
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