We are analyzing https://link.springer.com/article/10.1007/s11010-005-3454-9.

Title:
Ca2+-induced permeability transition in human lymphoblastoid cell mitochondria from normal and Huntington’s disease individuals | Molecular and Cellular Biochemistry
Description:
Huntington’s disease (HD) is associated with expansion of polyglutamine tract in a protein named huntingtin (htt) that is expressed in virtually all body tissues. Thus mutated htt (HD-htt) might affect all organs, although clinical manifestations of HD are associated with selective loss of corticostriatal neurons of the brain. In this work we studied how HD-htt affects mitochondria in human peripheral blood cells. We compared various functions of mitochondria isolated from cultured lymphoblastoid cells derived from three HD patients with juvenile onset of the disease (HD-LBM) and three age-matched control (C-LBM) individuals. Respiratory parameters in different metabolic states, with succinate and glutamate plus malate were the same for all control and HD cell lines. State 4 membrane potential in HD-LBM was slightly lower than in C-LBM. The calcium retention capacity (CRC) of mitochondria was estimated using simultaneously several methods to register permeability transition (PT). We found that LBM do not undergo swelling upon Ca2+-induced PT, and do not increase CRC in the presence of ADP + oligomycin. Although each cell line had different CRC values, qualitatively PT was different in C-LBM and HD-LBM. With C-LBM cyclosporin A (CsA) increased CRC significantly, while with HD-LBM CsA was ineffective. In C-LBM depolarization of mitochondria and a large pore opening (PT) always occurred simultaneously. In HD-LBM depolarization occurred at 20–50% lower Ca2+ loads than PT. We suggest that HD-htt promotes low H+ conductance of the mitochondria by interacting with proteins at the contacts sites without directly promoting PT or hampering mitochondrial oxidative phosphorylation. (Mol Cell Biochem 269: 143–152, 2005)
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Keywords {🔍}

google, scholar, mitochondrial, disease, mitochondria, huntingtons, permeability, article, transition, biophys, cell, panov, greenamyre, human, brain, biochem, membrane, apoptosis, huntingtin, calcium, pore, cas, pubmed, nature, liver, diseases, privacy, cookies, content, polyglutamine, cells, hdlbm, clbm, depolarization, pathogenesis, ann, biochim, acta, rat, channel, arch, publish, research, search, biochemistry, individuals, control, crc, access, neurosci,

Topics {✒️}

month download article/chapter calcium-induced permeability transition ca2+-induced permeability transition ca2+-dependent permeability transition calcium retention capacity wild-type huntingtin protects polyglutamine-expanded huntingtin activates hd-htt promotes low permeability transition pore hd-htt affects mitochondria human lymphoblast mitochondria privacy choices/manage cookies hd-lbm depolarization occurred ca2+-dependent depolarization full article pdf register permeability transition cellular biochemistry aims meta bolic research mitochondrial oxidative phosphorylation calcium-induced cytochrome adenine nucleotides carrier ca2+-induced pt total calcium concentrations large pore opening mitochondrial channel vdac powerful cyclosporin inhibition mitochondrial creatine kinase mitochondrial energy compromise membrane transport phenomena european economic area related subjects sek1-jnk pathway hereditary spastic paraplegia patient muscle biopsies adenine nucleotide translocase brown adipose tissue elsevier/north-holland energy metabolism defects reactive oxygen species striatal signaling genes emory university school transmitochondrial cell lines intracellular free calcium low-conductance channel ion channel formation ion channel hypothesis ca2+ imaging huntington' conditions privacy policy reduced mitochondrial function protein named huntingtin

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         headline:Ca2+-induced permeability transition in human lymphoblastoid cell mitochondria from normal and Huntington’s disease individuals
         description:Huntington’s disease (HD) is associated with expansion of polyglutamine tract in a protein named huntingtin (htt) that is expressed in virtually all body tissues. Thus mutated htt (HD-htt) might affect all organs, although clinical manifestations of HD are associated with selective loss of corticostriatal neurons of the brain. In this work we studied how HD-htt affects mitochondria in human peripheral blood cells. We compared various functions of mitochondria isolated from cultured lymphoblastoid cells derived from three HD patients with juvenile onset of the disease (HD-LBM) and three age-matched control (C-LBM) individuals. Respiratory parameters in different metabolic states, with succinate and glutamate plus malate were the same for all control and HD cell lines. State 4 membrane potential in HD-LBM was slightly lower than in C-LBM. The calcium retention capacity (CRC) of mitochondria was estimated using simultaneously several methods to register permeability transition (PT). We found that LBM do not undergo swelling upon Ca2+-induced PT, and do not increase CRC in the presence of ADP + oligomycin. Although each cell line had different CRC values, qualitatively PT was different in C-LBM and HD-LBM. With C-LBM cyclosporin A (CsA) increased CRC significantly, while with HD-LBM CsA was ineffective. In C-LBM depolarization of mitochondria and a large pore opening (PT) always occurred simultaneously. In HD-LBM depolarization occurred at 20–50% lower Ca2+ loads than PT. We suggest that HD-htt promotes low H+ conductance of the mitochondria by interacting with proteins at the contacts sites without directly promoting PT or hampering mitochondrial oxidative phosphorylation. (Mol Cell Biochem 269: 143–152, 2005)
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      headline:Ca2+-induced permeability transition in human lymphoblastoid cell mitochondria from normal and Huntington’s disease individuals
      description:Huntington’s disease (HD) is associated with expansion of polyglutamine tract in a protein named huntingtin (htt) that is expressed in virtually all body tissues. Thus mutated htt (HD-htt) might affect all organs, although clinical manifestations of HD are associated with selective loss of corticostriatal neurons of the brain. In this work we studied how HD-htt affects mitochondria in human peripheral blood cells. We compared various functions of mitochondria isolated from cultured lymphoblastoid cells derived from three HD patients with juvenile onset of the disease (HD-LBM) and three age-matched control (C-LBM) individuals. Respiratory parameters in different metabolic states, with succinate and glutamate plus malate were the same for all control and HD cell lines. State 4 membrane potential in HD-LBM was slightly lower than in C-LBM. The calcium retention capacity (CRC) of mitochondria was estimated using simultaneously several methods to register permeability transition (PT). We found that LBM do not undergo swelling upon Ca2+-induced PT, and do not increase CRC in the presence of ADP + oligomycin. Although each cell line had different CRC values, qualitatively PT was different in C-LBM and HD-LBM. With C-LBM cyclosporin A (CsA) increased CRC significantly, while with HD-LBM CsA was ineffective. In C-LBM depolarization of mitochondria and a large pore opening (PT) always occurred simultaneously. In HD-LBM depolarization occurred at 20–50% lower Ca2+ loads than PT. We suggest that HD-htt promotes low H+ conductance of the mitochondria by interacting with proteins at the contacts sites without directly promoting PT or hampering mitochondrial oxidative phosphorylation. (Mol Cell Biochem 269: 143–152, 2005)
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         human lymphoblast cells
         Huntington’s disease
         membrane potential
         mitochondria
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         Cancer Research
         Medical Biochemistry
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