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10.1074/jbc.M109.017731 http://scihub22266oqcxt.onion/10.1074/jbc.M109.017731 19880514!2804223!19880514     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19880514&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 500 Internal Server Error in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Biol+Chem 2010 ; 285 (1): 741-50 Nephropedia Template TP {{tp|p=19880514|t=2010. Increased potassium conductance of brain mitochondria induces resistance to permeability transition by enhancing matrix volume |pdf=|usr=}}{{19880514}} gab.com Text Increased potassium conductance of brain mitochondria induces resistance to permeability transition by enhancing matrix volume JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=19880514 #FOAvip Modulation of K(+) conductance of the inner mitochondrial membrane has been proposed to mediate preconditioning in ischemia-reperfusion injury. The mechanism is not entirely understood, but it has been linked to a decreased activation of mitochondrial permeability transition (mPT). In the present study K(+) channel activity was mimicked by picomolar concentrations of valinomycin. Isolated brain mitochondria were exposed to continuous infusions of calcium. Monitoring of extramitochondrial Ca(2+) and mitochondrial respiration provided a quantitative assay for mPT sensitivity by determining calcium retention capacity (CRC). Valinomycin and cyclophilin D inhibition separately and additively increased CRC. Comparable degrees of respiratory uncoupling induced by increased K(+) or H(+) conductance had opposite effects on mPT sensitivity. Protonophores dose-dependently decreased CRC, demonstrating that so-called mild uncoupling was not beneficial per se. The putative mitoK(ATP) channel opener diazoxide did not mimic the effect of valinomycin. An alkaline matrix pH was required for mitochondria to retain calcium, but increased K(+) conductance did not result in augmented DeltapH. The beneficial effect of valinomycin on CRC was not mediated by H(2)O(2)-induced protein kinase Cepsilon activation. Rather, increased K(+) conductance reduced H(2)O(2) generation during calcium infusion. Lowering the osmolarity of the buffer induced an increase in mitochondrial volume and improved CRC similar to valinomycin without inducing uncoupling or otherwise affecting respiration. We propose that increased potassium conductance in brain mitochondria may cause a direct physiological effect on matrix volume inducing resistance to pathological calcium challenges. Twit Text FOAVip Increased potassium conductance of brain mitochondria induces resistance to permeability transition by enhancing matrix volume ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=19880514 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19880514 #FOAvip English Wikipedia <ref>{{Cite pmid|19880514}}</ref> Increased potassium conductance of brain mitochondria induces resistance to permeability transition by enhancing matrix volume #MMPMID19880514 Hansson MJ; Morota S; Teilum M; Mattiasson G; Uchino H; Elmer E J Biol Chem 2010[Jan]; 285 (1): 741-50 PMID19880514show ga Modulation of K(+) conductance of the inner mitochondrial membrane has been proposed to mediate preconditioning in ischemia-reperfusion injury. The mechanism is not entirely understood, but it has been linked to a decreased activation of mitochondrial permeability transition (mPT). In the present study K(+) channel activity was mimicked by picomolar concentrations of valinomycin. Isolated brain mitochondria were exposed to continuous infusions of calcium. Monitoring of extramitochondrial Ca(2+) and mitochondrial respiration provided a quantitative assay for mPT sensitivity by determining calcium retention capacity (CRC). Valinomycin and cyclophilin D inhibition separately and additively increased CRC. Comparable degrees of respiratory uncoupling induced by increased K(+) or H(+) conductance had opposite effects on mPT sensitivity. Protonophores dose-dependently decreased CRC, demonstrating that so-called mild uncoupling was not beneficial per se. The putative mitoK(ATP) channel opener diazoxide did not mimic the effect of valinomycin. An alkaline matrix pH was required for mitochondria to retain calcium, but increased K(+) conductance did not result in augmented DeltapH. The beneficial effect of valinomycin on CRC was not mediated by H(2)O(2)-induced protein kinase Cepsilon activation. Rather, increased K(+) conductance reduced H(2)O(2) generation during calcium infusion. Lowering the osmolarity of the buffer induced an increase in mitochondrial volume and improved CRC similar to valinomycin without inducing uncoupling or otherwise affecting respiration. We propose that increased potassium conductance in brain mitochondria may cause a direct physiological effect on matrix volume inducing resistance to pathological calcium challenges. |*Mitochondrial Size/drug effects[MESH] |Alkalies/metabolism[MESH] |Animals[MESH] |Calcium/metabolism[MESH] |Carbonyl Cyanide m-Chlorophenyl Hydrazone/pharmacology[MESH] |Cell Respiration/drug effects[MESH] |Diazoxide/pharmacology[MESH] |Enzyme Activation/drug effects[MESH] |Hydrogen Peroxide/pharmacology[MESH] |Hydrogen-Ion Concentration/drug effects[MESH] |Hydrogen/metabolism[MESH] |Ion Transport/drug effects[MESH] |Male[MESH] |Mitochondria, Heart/drug effects/metabolism[MESH] |Mitochondria/*drug effects/*metabolism[MESH] |Mitochondrial Membrane Transport Proteins/*metabolism[MESH] |Mitochondrial Permeability Transition Pore[MESH] |Molecular Mimicry/drug effects[MESH] |Nigericin/pharmacology[MESH] |Potassium Channels/metabolism[MESH] |Potassium/*metabolism[MESH] |Protein Kinase C/metabolism[MESH] |Rats[MESH] |Rats, Wistar[MESH] |Reactive Oxygen Species/metabolism[MESH]Increased potassium conductance of brain mitochondria induces resistan(epmc).pdf DeepDyve Pubget Overpricing