The role of creatine kinase in inhibition of mitochondrial permeability transition
- PMID: 9315696
- DOI: 10.1016/s0014-5793(97)01045-4
The role of creatine kinase in inhibition of mitochondrial permeability transition
Abstract
Cyclosporin A sensitive swelling of mitochondria isolated from control mouse livers and from the livers of transgenic mice expressing human ubiquitous mitochondrial creatine kinase occurred in the presence of both 40 microM calcium and 5 microM atractyloside which was accompanied by a 2.5-fold increase over state 4 respiration rates. Creatine and cyclocreatine inhibited the latter only in transgenic liver mitochondria. Protein complexes isolated from detergent solubilised rat brain extracts, containing octameric mitochondrial creatine kinase, porin and the adenine nucleotide translocator, were reconstituted into malate loaded lipid vesicles. Dimerisation of creatine kinase in the complexes and exposure of the reconstituted complexes to >200 microM calcium induced a cyclosporin A sensitive malate release. No malate release occurred with complexes containing octameric creatine kinase under the same conditions.
Similar articles
-
Complexes between kinases, mitochondrial porin and adenylate translocator in rat brain resemble the permeability transition pore.FEBS Lett. 1996 Nov 4;396(2-3):189-95. doi: 10.1016/0014-5793(96)01092-7. FEBS Lett. 1996. PMID: 8914985
-
Complexes between porin, hexokinase, mitochondrial creatine kinase and adenylate translocator display properties of the permeability transition pore. Implication for regulation of permeability transition by the kinases.Biochim Biophys Acta. 1998 Jan 5;1368(1):7-18. doi: 10.1016/s0005-2736(97)00175-2. Biochim Biophys Acta. 1998. PMID: 9459579
-
Inhibition of Ca2(+)-induced large-amplitude swelling of liver and heart mitochondria by cyclosporin is probably caused by the inhibitor binding to mitochondrial-matrix peptidyl-prolyl cis-trans isomerase and preventing it interacting with the adenine nucleotide translocase.Biochem J. 1990 May 15;268(1):153-60. doi: 10.1042/bj2680153. Biochem J. 1990. PMID: 2160810 Free PMC article.
-
The molecular structure of mitochondrial contact sites. Their role in regulation of energy metabolism and permeability transition.Biofactors. 1998;8(3-4):235-42. doi: 10.1002/biof.5520080311. Biofactors. 1998. PMID: 9914825 Review.
-
Mitochondrial creatine kinase in contact sites: interaction with porin and adenine nucleotide translocase, role in permeability transition and sensitivity to oxidative damage.Biol Signals Recept. 2001 Jan-Apr;10(1-2):93-111. doi: 10.1159/000046878. Biol Signals Recept. 2001. PMID: 11223643 Review.
Cited by
-
The potential role of creatine supplementation in neurodegenerative diseases.Phys Act Nutr. 2023 Dec;27(4):48-54. doi: 10.20463/pan.2023.0037. Epub 2023 Dec 31. Phys Act Nutr. 2023. PMID: 38297476 Free PMC article.
-
Additive neuroprotective effects of creatine and a cyclooxygenase 2 inhibitor against dopamine depletion in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease.J Mol Neurosci. 2003;21(3):191-8. doi: 10.1385/jmn:21:3:191. J Mol Neurosci. 2003. PMID: 14645986
-
Neuroprotective effects of creatine in a transgenic mouse model of Huntington's disease.J Neurosci. 2000 Jun 15;20(12):4389-97. doi: 10.1523/JNEUROSCI.20-12-04389.2000. J Neurosci. 2000. PMID: 10844007 Free PMC article.
-
The failure of mitochondria leads to neurodegeneration: Do mitochondria need a jump start?Adv Drug Deliv Rev. 2009 Nov 30;61(14):1316-23. doi: 10.1016/j.addr.2009.07.016. Epub 2009 Aug 27. Adv Drug Deliv Rev. 2009. PMID: 19716395 Free PMC article. Review.
-
Prophylactic creatine administration mediates neuroprotection in cerebral ischemia in mice.J Neurosci. 2004 Jun 30;24(26):5909-12. doi: 10.1523/JNEUROSCI.1278-04.2004. J Neurosci. 2004. PMID: 15229238 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
