Bioenergetic characterization of mouse podocytes
Identifieur interne : 000795 ( Main/Exploration ); précédent : 000794; suivant : 000796Bioenergetic characterization of mouse podocytes
Auteurs : Yoshifusa Abe [États-Unis, Japon] ; Toru Sakairi [États-Unis] ; Hiroshi Kajiyama [Japon] ; Shashi Shrivastav [États-Unis] ; Craig Beeson [États-Unis] ; Jeffrey B. Kopp [États-Unis]Source :
- American journal of physiology. Cell physiology [ 0363-6143 ] ; 2010.
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- Pascal (Inist)
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- topic : Acidification.
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Abstract
Mitochondrial dysfunction contributes to podocyte injury, but normal podocyte bioenergetics have not been characterized. We measured oxygen consumption rates (OCR) and extracellular acidification rates (ECAR), using a transformed mouse podocyte cell line and the Seahorse Bioscience XF24 Extracellular Flux Analyzer. Basal OCR and ECAR were 55.2 ± 9.9 pmol/min and 3.1 ± 1.9 milli-pH units/min, respectively. The complex V inhibitor oligomycin reduced OCR to ∼45% of baseline rates, indicating that ∼55% of cellular oxygen consumption was coupled to ATP synthesis. Rotenone, a complex I inhibitor, reduced OCR to ∼25% of the baseline rates, suggesting that mitochondrial respiration accounted for ∼75% of the total cellular respiration. Thus ∼75% of mitochondrial respiration was coupled to ATP synthesis and ∼25% was accounted for by proton leak. Carbonyl cyanide p-trifluorome-thoxyphenylhydrazone (FCCP), which uncouples electron transport from ATP generation, increased OCR and ECAR to ∼360% and 840% of control levels. FCCP plus rotenone reduced ATP content by 60%, the glycolysis inhibitor 2-deoxyglucose reduced ATP by 35%, and 2-deoxyglucose in combination with FCCP or rotenone reduced ATP by >85%. The lactate dehydrogenase inhibitor oxamate and 2-deoxyglucose did not reduce ECAR, and 2-deoxyglucose had no effect on OCR, although 2-deoxyglucose reduced ATP content by 25%. Mitochondrial uncoupling induced by FCCP was associated with increased OCR with certain substrates, including lactate, glucose, pyruvate, and palmitate. Replication of these experiments in primary mouse podocytes yielded similar data. We conclude that mitochondria play the primary role in maintaining podocyte energy homeostasis, while glycolysis makes a lesser contribution.
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Kopp</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Maryland</region></placeName></affiliation></author></analytic><series><title level="j" type="main">American journal of physiology. Cell physiology</title><title level="j" type="abbreviated">Am. j. physiol., Cell physiol.</title><idno type="ISSN">0363-6143</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">American journal of physiology. Cell physiology</title><title level="j" type="abbreviated">Am. j. physiol., Cell physiol.</title><idno type="ISSN">0363-6143</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acidification</term><term>Extracellular</term><term>Mitochondria</term><term>Mouse</term><term>Oxygen consumption</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Mitochondrie</term><term>Consommation oxygène</term><term>Extracellulaire</term><term>Acidification</term><term>Souris</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Acidification</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mitochondrial dysfunction contributes to podocyte injury, but normal podocyte bioenergetics have not been characterized. We measured oxygen consumption rates (OCR) and extracellular acidification rates (ECAR), using a transformed mouse podocyte cell line and the Seahorse Bioscience XF24 Extracellular Flux Analyzer. Basal OCR and ECAR were 55.2 ± 9.9 pmol/min and 3.1 ± 1.9 milli-pH units/min, respectively. The complex V inhibitor oligomycin reduced OCR to ∼45% of baseline rates, indicating that ∼55% of cellular oxygen consumption was coupled to ATP synthesis. Rotenone, a complex I inhibitor, reduced OCR to ∼25% of the baseline rates, suggesting that mitochondrial respiration accounted for ∼75% of the total cellular respiration. Thus ∼75% of mitochondrial respiration was coupled to ATP synthesis and ∼25% was accounted for by proton leak. Carbonyl cyanide p-trifluorome-thoxyphenylhydrazone (FCCP), which uncouples electron transport from ATP generation, increased OCR and ECAR to ∼360% and 840% of control levels. FCCP plus rotenone reduced ATP content by 60%, the glycolysis inhibitor 2-deoxyglucose reduced ATP by 35%, and 2-deoxyglucose in combination with FCCP or rotenone reduced ATP by >85%. The lactate dehydrogenase inhibitor oxamate and 2-deoxyglucose did not reduce ECAR, and 2-deoxyglucose had no effect on OCR, although 2-deoxyglucose reduced ATP content by 25%. Mitochondrial uncoupling induced by FCCP was associated with increased OCR with certain substrates, including lactate, glucose, pyruvate, and palmitate. Replication of these experiments in primary mouse podocytes yielded similar data. We conclude that mitochondria play the primary role in maintaining podocyte energy homeostasis, while glycolysis makes a lesser contribution.</div></front></TEI><affiliations><list><country><li>Japon</li><li>États-Unis</li></country><region><li>Caroline du Sud</li><li>Maryland</li></region><settlement><li>Tokyo</li></settlement></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Abe, Yoshifusa" sort="Abe, Yoshifusa" uniqKey="Abe Y" first="Yoshifusa" last="Abe">Yoshifusa Abe</name></region><name sortKey="Beeson, Craig" sort="Beeson, Craig" uniqKey="Beeson C" first="Craig" last="Beeson">Craig Beeson</name><name sortKey="Kopp, Jeffrey B" sort="Kopp, Jeffrey B" uniqKey="Kopp J" first="Jeffrey B." last="Kopp">Jeffrey B. Kopp</name><name sortKey="Sakairi, Toru" sort="Sakairi, Toru" uniqKey="Sakairi T" first="Toru" last="Sakairi">Toru Sakairi</name><name sortKey="Shrivastav, Shashi" sort="Shrivastav, Shashi" uniqKey="Shrivastav S" first="Shashi" last="Shrivastav">Shashi Shrivastav</name></country><country name="Japon"><noRegion><name sortKey="Abe, Yoshifusa" sort="Abe, Yoshifusa" uniqKey="Abe Y" first="Yoshifusa" last="Abe">Yoshifusa Abe</name></noRegion><name sortKey="Kajiyama, Hiroshi" sort="Kajiyama, Hiroshi" uniqKey="Kajiyama H" first="Hiroshi" last="Kajiyama">Hiroshi Kajiyama</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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