NDLI: Ca2+ overload and mitochondrial permeability transition pore activation in living delta-sarcoglycan-deficient cardiomyocytes.

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Ca2+ overload and mitochondrial permeability transition pore activation in living delta-sarcoglycan-deficient cardiomyocytes.

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Ca2+ overload and mitochondrial permeability transition pore activation in living delta-sarcoglycan-deficient cardiomyocytes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Fraysse, Bodvaël Nagi, Sadia M. Boher, Belinda Ragot, Hélène Lainé, Jeanne Salmon, André Fiszman, Marc Y. Toussaint, Marcel Fromes, Yves
Description	Country affiliation: France Author Affiliation: Fraysse B ( Institut de Myologie-UPMC, INSERM U974, CNRS, Paris, France.)
Abstract	Muscular dystrophies are often associated with significant cardiac disease that can be the prominent feature associated with gene mutations in sarcoglycan. Cardiac cell death is a main feature of cardiomyopathy in sarcoglycan deficiency and may arise as a cardiomyocyte intrinsic process that remains unclear. Deficiency of delta-sarcoglycan (delta-SG) induces disruption of the dystrophin-associated glycoprotein complex, a known cause of membrane instability that may explain cardiomyocytes cytosolic Ca2+ increase. In this study we assessed the hypothesis that cytosolic Ca2+ increase triggers cardiomyocyte death through mitochondrial Ca2+ overload and dysfunction in the delta-SG-deficient CHF147 hamster. We showed that virtually all isolated CHF147 ventricular myocytes exhibited elevated cytosolic and mitochondrial Ca2+ levels by the use of the Fura-2 and Rhod-2 fluorescent probes. Observation of living cells with Mito-Tracker red lead to the conclusion that approximately 15% of isolated CHF147 cardiomyocytes had disorganized mitochondria. Transmission electron microscope imaging showed mitochondrial swelling associated with crest and membrane disruption. Analysis of the mitochondrial permeability transition pore (MPTP) activity using calcein revealed that mitochondria of CHF147 ventricular cells were twofold leakier than wild types, whereas reactive oxygen species production was unchanged. Bax, Bcl-2, and LC3 expression analysis by Western blot indicated that the intrinsic apoptosis and the cell death associated to autophagy pathways were not significantly activated in CHF147 hearts. Our results lead to conclusion that cardiomyocytes death in delta-SG-deficient animals is an intrinsic phenomenon, likely related to Ca2+-induced necrosis. In this process Ca2+ overload-induced MPTP activation and mitochondrial disorganization may have an important role.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
Journal	American Journal of Physiology - Cell Physiology
Issue Number	3
Volume Number	299
Language	English
Publisher	American Physiological Society
Publisher Date	2010-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Calcium Metabolism Mitochondrial Membrane Transport Proteins Myocytes, Cardiac Sarcoglycans Animals Cell Death Cricetinae Cytosol Heart Ventricles Cytology In Vitro Techniques Mesocricetus Microtubule-associated Proteins Biosynthesis Mitochondria Ultrastructure Proto-oncogene Proteins C-bcl-2 Reactive Oxygen Species Genetics Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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