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Difference between revisions of "Thomas 2011 Mitochondrion"

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{{Publication
{{Publication
|title=Thomas RR, Khan SM, Portell FR, Smigrodzki RM, Bennett JP Jr (2011) Recombinant human mitochondrial transcription factor A stimulates mitochondrial biogenesis and ATP synthesis, improves motor function after MPTP, reduces oxidative stress and increases survival after endotoxin. Mitochondrion 11: 108-118.
|title=Thomas RR, Khan SM, Portell FR, Smigrodzki RM, Bennett JP Jr (2011) Recombinant human mitochondrial transcription factor A stimulates mitochondrial biogenesis and ATP synthesis, improves motor function after MPTP, reduces oxidative stress and increases survival after endotoxin. Mitochondrion 11:108-18.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/20727424 PMID:20727424 ]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/20727424 PMID: 20727424 Open Access]
|authors=Thomas RR, Khan SM, Portell FR, Smigrodzki RM, Bennett JP
|authors=Thomas RR, Khan SM, Portell FR, Smigrodzki RM, Bennett JP
|year=2011
|year=2011
|journal=Mitochondrion
|journal=Mitochondrion
|abstract=Recombinant human mitochondrial transcription factor A protein (rhTFAM) was evaluated for its acute effects on cultured cells and chronic effects in mice. Fibroblasts incubated with rhTFAM acutely increased respiration in a chloramphenicol-sensitive manner. SH-SY5Y cells showed rhTFAM concentration-dependent reduction of methylpyridinium (MPP+)-induced oxidative stress and increases in lowered ATP levels and viability. Mice treated with weekly i.v. rhTFAM showed increased mitochondrial gene copy number, Complex I protein levels and ATP production rates; oxidative damage to proteins was decreased ~50%. rhTFAM treatment improved motor recovery rate after treatment with MPTP and dose-dependently improved survival in the lipopolysaccharide model of endotoxin sepsis.
|abstract=Recombinant human mitochondrial transcription factor A protein (rhTFAM) was evaluated for its acute effects on cultured cells and chronic effects in mice. Fibroblasts incubated with rhTFAM acutely increased respiration in a chloramphenicol-sensitive manner. SH-SY5Y cells showed rhTFAM concentration-dependent reduction of methylpyridinium (MPP+)-induced oxidative stress and increases in lowered ATP levels and viability. Mice treated with weekly i.v. rhTFAM showed increased mitochondrial gene copy number, Complex I protein levels and ATP production rates; oxidative damage to proteins was decreased ~50%. rhTFAM treatment improved motor recovery rate after treatment with MPTP and dose-dependently improved survival in the lipopolysaccharide model of endotoxin sepsis.
|keywords=recombinant TFAM, mitochondrial biogenesis, ATP synthesis, MPTP, sepsis
|keywords=Recombinant TFAM, Mitochondrial biogenesis, ATP synthesis, MPTP, Sepsis
|mipnetlab=US_VA Richmond_Bennett JP, US VA Richmond Virginia Commonwealth Univ
|mipnetlab=US VA Richmond Bennett JP, US VA Richmond Iyer S
}}
}}
{{Labeling
{{Labeling
|injuries=Oxidative stress;RONS
|organism=Human, Mouse
|tissues=Heart, Skeletal muscle, Nervous system, Fibroblast
|preparations=Homogenate, Isolated mitochondria
|topics=ATP, ATP production
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|injuries=RONS; Oxidative Stress
|organism=Human, Mouse
|tissues=Cardiac muscle, Skeletal muscle, Nervous system
|model cell lines=Fibroblast
|preparations=Homogenate, Isolated Mitochondria
|topics=ATP; ADP; AMP; PCr
}}
}}

Latest revision as of 15:36, 9 November 2016

Publications in the MiPMap
Thomas RR, Khan SM, Portell FR, Smigrodzki RM, Bennett JP Jr (2011) Recombinant human mitochondrial transcription factor A stimulates mitochondrial biogenesis and ATP synthesis, improves motor function after MPTP, reduces oxidative stress and increases survival after endotoxin. Mitochondrion 11:108-18.

Β» PMID: 20727424 Open Access

Thomas RR, Khan SM, Portell FR, Smigrodzki RM, Bennett JP (2011) Mitochondrion

Abstract: Recombinant human mitochondrial transcription factor A protein (rhTFAM) was evaluated for its acute effects on cultured cells and chronic effects in mice. Fibroblasts incubated with rhTFAM acutely increased respiration in a chloramphenicol-sensitive manner. SH-SY5Y cells showed rhTFAM concentration-dependent reduction of methylpyridinium (MPP+)-induced oxidative stress and increases in lowered ATP levels and viability. Mice treated with weekly i.v. rhTFAM showed increased mitochondrial gene copy number, Complex I protein levels and ATP production rates; oxidative damage to proteins was decreased ~50%. rhTFAM treatment improved motor recovery rate after treatment with MPTP and dose-dependently improved survival in the lipopolysaccharide model of endotoxin sepsis. β€’ Keywords: Recombinant TFAM, Mitochondrial biogenesis, ATP synthesis, MPTP, Sepsis

β€’ O2k-Network Lab: US VA Richmond Bennett JP, US VA Richmond Iyer S


Labels:

Stress:Oxidative stress;RONS  Organism: Human, Mouse  Tissue;cell: Heart, Skeletal muscle, Nervous system, Fibroblast  Preparation: Homogenate, Isolated mitochondria 

Regulation: ATP, ATP production 


HRR: Oxygraph-2k