Passive Ca(2+) overload in H9c2 cardiac myoblasts: assessment of cellular damage and cytosolic Ca(2+) transients

Lax Pérez, Antonio Manuel; Asensio López, María del Carmen; Pascual Figal, Domingo Andrés; Fernandez Belda, Francisco; Soler Pardo, Fernando

Publication:
Passive Ca(2+) overload in H9c2 cardiac myoblasts: assessment of cellular damage and cytosolic Ca(2+) transients

dc.contributor.author	Lax Pérez, Antonio Manuel
dc.contributor.author	Asensio López, María del Carmen
dc.contributor.author	Pascual Figal, Domingo Andrés
dc.contributor.author	Fernandez Belda, Francisco
dc.contributor.author	Soler Pardo, Fernando
dc.contributor.department	Medicina
dc.date.accessioned	2024-07-15T11:21:58Z
dc.date.available	2024-07-15T11:21:58Z
dc.date.issued	2011-08-15
dc.description	© 2011 Elsevier Inc. This document is the Published version of a Published Work that appeared in final form in Archives of Biochemistry and Biophysics. To access the final edited and published work see https://doi.org/10.1016/j.abb.2011.05.019
dc.description.abstract	Increase of resting Ca(2+) levels and amplitude of vasopressin-induced Ca(2+) transients were observed when cells in serum-free medium were exposed to 5mM Ca(2+) for 2h. Small effect on cell viability was also observed. A rapid cytotoxic effect was developed in the presence of 10mM Ca(2+) and absence of serum. However, cells exposed to 10mM Ca(2+) in the presence of serum were protected from damage for at least 2days. Resting Ca(2+) levels and cytosolic Ca(2+) transients in serum-containing medium with 10mM Ca(2+) displayed lower increases and a tendency to recover control values. When serum was absent, cells preincubated with 10mM Ca(2+) were more sensitive to thapsigargin-induced damage than cells preincubated with lower Ca(2+). The sensitivity was similar when serum was present. Tolerance to high Ca(2+) in the presence of serum was linked to potentiation of the mitochondrial Ca(2+) entry to decrease the sarcoplasmic reticulum Ca(2+) overload.	es
dc.format	application/pdf	es
dc.format.extent	8	es
dc.identifier.citation	Archives of Biochemistry and Biophysics, 2011, Vol. 512, Issue 2, pp. 175-182
dc.identifier.doi	https://doi.org/10.1016/j.abb.2011.05.019
dc.identifier.issn	Print: 0003-9861
dc.identifier.issn	Electronic: 1096-0384
dc.identifier.uri	http://hdl.handle.net/10201/143112
dc.language	eng	es
dc.publisher	Elsevier
dc.relation	This study was supported by Grant BMC2002-02474 from the Spanish Ministerio de Educación y Cultura and a grant-in-aid from the Universidad de Murcia to F.F.B. and by Grant 11857/PI/09 from Fundación Séneca Región de Murcia, Spain to D.P.F.	es
dc.relation.publisherversion	https://www.sciencedirect.com/science/article/pii/S0003986111001913#aep-acknowledgment-id19
dc.rights.accessRights	info:eu-repo/semantics/restrictedAccess
dc.subject	Sarcoplasmic reticulum	es
dc.subject	Thapsigargin	es
dc.subject	Ca2+ overload	es
dc.subject	Ca2+ transient	es
dc.subject	Cell damage	es
dc.subject	H9c2 cell	es
dc.title	Passive Ca(2+) overload in H9c2 cardiac myoblasts: assessment of cellular damage and cytosolic Ca(2+) transients	es
dc.type	info:eu-repo/semantics/article	es
dspace.entity.type	Publication	es
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