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Can J Physiol Pharmacol. 2013 Nov;91(11):966-72. doi: 10.1139/cjpp-2013-0113. Epub 2013 Jul 17.

Parvalbumin is overexpressed in the late phase of pharmacological preconditioning in skeletal muscle.

Author information

1
Departamento de Farmacología. Centro de Investigación y de Estudios Avanzados del I.P.N., México, D.F. 07360.

Abstract

Pharmacological preconditioning (PPC) with mitochondrial ATP-sensitive K(+) channel openers such as diazoxide, provides protection against ischemia in cardiac muscle, skeletal muscle, and other tissues. Effects on Ca(2+) homeostasis during the late phase of PPC have been described in cardiomyocytes, but no information is available regarding intracellular Ca(2+) changes in skeletal muscle fibers during late PPC. Intracellular Ca(2+) signals were measured in single fibers of adult mouse skeletal muscle, with fluorescent probes, 48 h after the administration of diazoxide. Parvalbumin levels in the myofibers were quantitated by Western blot. Diazoxide induction of late PPC was confirmed by partial protection of muscles from peroxide-induced damage. Late PPC was associated with a significant decrease in the duration of Ca(2+) signals during single twitches and tetanus with no changes in peak values. This effect was prevented by the reactive oxygen species (ROS) scavenger tiron. Late PPC was accompanied by a 30% increase in parvalbumin levels, and this effect was also blocked by tiron. Our data show, for the first time, a role of parvalbumin in late PPC in skeletal muscle.

PMID:
24117265
DOI:
10.1139/cjpp-2013-0113
[Indexed for MEDLINE]

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