Redox regulation of calcium release in skeletal and cardiac muscle

In skeletal and cardiac muscle cells, specific isoforms of the Ryanodine receptor channels mediate Ca2+ release from the sarcoplasmic reticulum. These channels are highly susceptible to redox modifications, which regulate channel activity. In this work, we studied the effects of Ca2+ (endogenous ago...

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Autores principales:	HIDALGO,CECILIA, ARACENA,PAULA, SANCHEZ,GINA, DONOSO,PAULINA
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2002
Materias:	Redox state Ryanodine receptors sarcoplasmic reticulum calcium release kinetics Mg2+ inhibition S-nitrosoglutathione
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602002000200009
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spelling	oai:scielo:S0716-976020020002000092002-12-26Redox regulation of calcium release in skeletal and cardiac muscleHIDALGO,CECILIAARACENA,PAULASANCHEZ,GINADONOSO,PAULINA Redox state Ryanodine receptors sarcoplasmic reticulum calcium release kinetics Mg2+ inhibition S-nitrosoglutathione In skeletal and cardiac muscle cells, specific isoforms of the Ryanodine receptor channels mediate Ca2+ release from the sarcoplasmic reticulum. These channels are highly susceptible to redox modifications, which regulate channel activity. In this work, we studied the effects of Ca2+ (endogenous agonist) and Mg2+ (endogenous inhibitor) on the kinetics of Ca2+ release from sarcoplasmic reticulum vesicles isolated from skeletal or cardiac mammalian muscle. Native skeletal vesicles exhibited maximal stimulation of release kinetics by 10-20 µM [Ca2+], whereas in native cardiac vesicles, maximal stimulation of release required only 1 µM [Ca2+]. In 10 µM [Ca2+], free [Mg2+] < 0.1 mM produced marked inhibition of release from skeletal vesicles but free [Mg2+] 0.8 mM did not affect release from cardiac vesicles. Incubation of skeletal or cardiac vesicles with the oxidant thimerosal increased their susceptibility to stimulation by Ca2+ and decreased the inhibitory effect of Mg2+ in skeletal vesicles. Sulfhydryl-reducing agents fully reversed the effects of thimerosal. The endogenous redox species, glutathione disulfide and S-nitrosoglutathione, also stimulated release from skeletal sarcoplasmic reticulum vesicles. In 10 µM [Ca2+], 35S-nitrosoglutathione labeled a protein fraction enriched in release channels through S-glutathiolation. Free [Mg2+] 1 mM or decreasing free [Ca2+] to the nM range prevented this reaction. Possible physiological and pathological consequences of redox modification of release channels on Ca2+ signaling in heart and muscle cells are discussedinfo:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.35 n.2 20022002-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602002000200009en10.4067/S0716-97602002000200009
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	Redox state Ryanodine receptors sarcoplasmic reticulum calcium release kinetics Mg2+ inhibition S-nitrosoglutathione
spellingShingle	Redox state Ryanodine receptors sarcoplasmic reticulum calcium release kinetics Mg2+ inhibition S-nitrosoglutathione HIDALGO,CECILIA ARACENA,PAULA SANCHEZ,GINA DONOSO,PAULINA Redox regulation of calcium release in skeletal and cardiac muscle
description	In skeletal and cardiac muscle cells, specific isoforms of the Ryanodine receptor channels mediate Ca2+ release from the sarcoplasmic reticulum. These channels are highly susceptible to redox modifications, which regulate channel activity. In this work, we studied the effects of Ca2+ (endogenous agonist) and Mg2+ (endogenous inhibitor) on the kinetics of Ca2+ release from sarcoplasmic reticulum vesicles isolated from skeletal or cardiac mammalian muscle. Native skeletal vesicles exhibited maximal stimulation of release kinetics by 10-20 µM [Ca2+], whereas in native cardiac vesicles, maximal stimulation of release required only 1 µM [Ca2+]. In 10 µM [Ca2+], free [Mg2+] < 0.1 mM produced marked inhibition of release from skeletal vesicles but free [Mg2+] 0.8 mM did not affect release from cardiac vesicles. Incubation of skeletal or cardiac vesicles with the oxidant thimerosal increased their susceptibility to stimulation by Ca2+ and decreased the inhibitory effect of Mg2+ in skeletal vesicles. Sulfhydryl-reducing agents fully reversed the effects of thimerosal. The endogenous redox species, glutathione disulfide and S-nitrosoglutathione, also stimulated release from skeletal sarcoplasmic reticulum vesicles. In 10 µM [Ca2+], 35S-nitrosoglutathione labeled a protein fraction enriched in release channels through S-glutathiolation. Free [Mg2+] 1 mM or decreasing free [Ca2+] to the nM range prevented this reaction. Possible physiological and pathological consequences of redox modification of release channels on Ca2+ signaling in heart and muscle cells are discussed
author	HIDALGO,CECILIA ARACENA,PAULA SANCHEZ,GINA DONOSO,PAULINA
author_facet	HIDALGO,CECILIA ARACENA,PAULA SANCHEZ,GINA DONOSO,PAULINA
author_sort	HIDALGO,CECILIA
title	Redox regulation of calcium release in skeletal and cardiac muscle
title_short	Redox regulation of calcium release in skeletal and cardiac muscle
title_full	Redox regulation of calcium release in skeletal and cardiac muscle
title_fullStr	Redox regulation of calcium release in skeletal and cardiac muscle
title_full_unstemmed	Redox regulation of calcium release in skeletal and cardiac muscle
title_sort	redox regulation of calcium release in skeletal and cardiac muscle
publisher	Sociedad de Biología de Chile
publishDate	2002
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602002000200009
work_keys_str_mv	AT hidalgocecilia redoxregulationofcalciumreleaseinskeletalandcardiacmuscle AT aracenapaula redoxregulationofcalciumreleaseinskeletalandcardiacmuscle AT sanchezgina redoxregulationofcalciumreleaseinskeletalandcardiacmuscle AT donosopaulina redoxregulationofcalciumreleaseinskeletalandcardiacmuscle
_version_	1718441340322185216

Redox regulation of calcium release in skeletal and cardiac muscle

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