PUBLICATION
Mitochondrial Ca(2+) transport and permeability transition in zebrafish (Danio rerio)
- Authors
- Azzolin, L., Basso, E., Argenton, F., and Bernardi, P.
- ID
- ZDB-PUB-100719-65
- Date
- 2010
- Source
- Biochimica et biophysica acta. Gene regulatory mechanisms 1797(11): 1775-1779 (Journal)
- Registered Authors
- Argenton, Francesco
- Keywords
- none
- MeSH Terms
-
- Animals
- Calcium/metabolism*
- Calcium Channel Blockers/pharmacology
- Cell Death/drug effects
- Cell Membrane Permeability/physiology*
- Cells, Cultured
- Cyclosporine/pharmacology
- Embryo, Nonmammalian/cytology
- Embryo, Nonmammalian/drug effects
- Embryo, Nonmammalian/metabolism*
- Female
- Immunosuppressive Agents/pharmacology
- Male
- Membrane Potential, Mitochondrial/drug effects
- Membrane Potential, Mitochondrial/physiology
- Mitochondria/drug effects
- Mitochondria/metabolism*
- Mitochondrial Membrane Transport Proteins/drug effects
- Mitochondrial Membrane Transport Proteins/metabolism*
- Zebrafish
- PubMed
- 20633532 Full text @ BBA Gene Regulatory Mechanisms
Citation
Azzolin, L., Basso, E., Argenton, F., and Bernardi, P. (2010) Mitochondrial Ca(2+) transport and permeability transition in zebrafish (Danio rerio). Biochimica et biophysica acta. Gene regulatory mechanisms. 1797(11):1775-1779.
Abstract
We have studied mitochondrial Ca(2+) transport and the permeability transition (PT) in the teleost zebrafish (Danio rerio), a key model system for human diseases. Permeabilized zebrafish embryo cells displayed a mitochondrial energy-dependent Ca(2+) uptake system that, like the Ca(2+) uniporter of mammals, was inhibited by ruthenium red. Zebrafish mitochondria underwent a Ca(2+)-dependent PT that displayed Pi-dependent desensitization by cyclosporin A, and responded appropriately to key modulators of the mammalian PT pore (voltage, pH, ubiquinone 0, dithiol oxidants and cross linkers, ligands of the adenine nucleotide translocator, arachidonic acid). Opening of the pore was documented in intact cells, where it led to death that could largely be prevented by cyclosporin A. Our results represent a necessary step toward the use of zebrafish for the screening and validation of PTP inhibitors of potential use in human diseases, as recently shown for collagen VI muscular dystrophy [W.R. Telfer et al., Zebrafish models of collagen VI related myopathies, Hum. Mol. Genet. 19 (2010) 2433-2444].
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping