Mitochondrial electron transport and glycolysis are coupled in articular cartilage
Summary Objective Although the majority of the adenosine triphosphate (ATP) in chondrocytes is made by glycolysis rather than by oxidative phosphorylation in mitochondria there is evidence to suggest that reactive oxygen species produced by mitochondrial electron transport (ET) help to maintain cell...
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| Veröffentlicht in: | Osteoarthritis and cartilage 2012-04, Vol.20 (4), p.323-329 |
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| creator | Martin, J.A Martini, A Molinari, A Morgan, W Ramalingam, W Buckwalter, J.A McKinley, T.O |
| description | Summary Objective Although the majority of the adenosine triphosphate (ATP) in chondrocytes is made by glycolysis rather than by oxidative phosphorylation in mitochondria there is evidence to suggest that reactive oxygen species produced by mitochondrial electron transport (ET) help to maintain cellular redox balance in favor of glycolysis. The objective of this study was to test this hypothesis by determining if rotenone, which inhibits ET and blocks oxidant production inhibits glycolytic ATP synthesis. Design Bovine osteochondral explants were treated with rotenone, an ET inhibitor; or oligomycin an ATP synthase inhibitor; or 2-fluoro-2-deoxy- d -glucose, a glycolysis inhibiter; or peroxide, an exogenous oxidant; or mitoquinone (MitoQ), a mitochondria-targeted anti-oxidant. Cartilage extracts were assayed for ATP, nicotine adenine dinucleotide (NAD+/H), and culture medium was assayed for pyruvate and lactate after 24 h of treatment. Imaging studies were used to measure superoxide production in cartilage. Results Rotenone and 2-FG caused a significant decline in cartilage ATP ( P |
| doi_str_mv | 10.1016/j.joca.2012.01.003 |
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| fullrecord | <record><control><sourceid>elsevier_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3634328</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>1_s2_0_S1063458412000246</els_id><sourcerecordid>1_s2_0_S1063458412000246</sourcerecordid><originalsourceid>FETCH-LOGICAL-c509t-a5dd2ab938e6ab7c6390fe263232007bdad35423fe3b174e98c58d10c73208f13</originalsourceid><addsrcrecordid>eNp9kdFq3DAQRUVpaNK0P9CH4B-wO5Jsrw0lUELSFhICafMs5NF4I0eRFsm7sH8fmU1D24c-acTce0c6w9gnDhUH3n6eqimgrgRwUQGvAOQbdsIbIcq-beTbXEMry7rp6mP2PqUJsoJzeMeOhZDQ9H1_wu5u7BzwIXgTrXYFOcI5Bl_MUfu0CXEutDfF2u0xuH2yqdCRCgzbjSNTWJ-vs8Wt07HApXR6TR_Y0ahdoo8v5ym7v7r8dfG9vL799uPi63WJDfRzqRtjhB562VGrhxW2soeRRCuFFACrwWgjm1rIkeTAVzX1HTad4YCr3O9GLk_Z-SF3sx2eyCD5_GinNtE-6bhXQVv1d8fbB7UOOyVbWUvR5QBxCMAYUoo0vno5qIWwmtRCWC2EFXCV-WXT2Z9TXy2_kWbBl4OA8t93lqJKaMkjGRszXGWC_X_--T92dNZb1O6R9pSmsI0-U1VcpexRP5cdLyvmGRqIupXPma2kDA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Mitochondrial electron transport and glycolysis are coupled in articular cartilage</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Martin, J.A ; Martini, A ; Molinari, A ; Morgan, W ; Ramalingam, W ; Buckwalter, J.A ; McKinley, T.O</creator><creatorcontrib>Martin, J.A ; Martini, A ; Molinari, A ; Morgan, W ; Ramalingam, W ; Buckwalter, J.A ; McKinley, T.O</creatorcontrib><description>Summary Objective Although the majority of the adenosine triphosphate (ATP) in chondrocytes is made by glycolysis rather than by oxidative phosphorylation in mitochondria there is evidence to suggest that reactive oxygen species produced by mitochondrial electron transport (ET) help to maintain cellular redox balance in favor of glycolysis. The objective of this study was to test this hypothesis by determining if rotenone, which inhibits ET and blocks oxidant production inhibits glycolytic ATP synthesis. Design Bovine osteochondral explants were treated with rotenone, an ET inhibitor; or oligomycin an ATP synthase inhibitor; or 2-fluoro-2-deoxy- d -glucose, a glycolysis inhibiter; or peroxide, an exogenous oxidant; or mitoquinone (MitoQ), a mitochondria-targeted anti-oxidant. Cartilage extracts were assayed for ATP, nicotine adenine dinucleotide (NAD+/H), and culture medium was assayed for pyruvate and lactate after 24 h of treatment. Imaging studies were used to measure superoxide production in cartilage. Results Rotenone and 2-FG caused a significant decline in cartilage ATP ( P < 0.001). In contrast, ATP levels were not affected by oligomycin. Peroxide treatment blocked rotenone effects on ATP, while treatment with MitoQ significantly suppressed ATP levels. Rotenone and 2-FG caused a significant decline in pyruvate, but not in lactate production. NADH:NAD+ ratios decreased significantly in both rotenone and 2-FG-treated explants ( P < 0.05). Rotenone also significantly reduced superoxide production. Conclusions These findings showing a link between glycolysis and ET are consistent with previous reports on the critical need for oxidants to support normal chondrocyte metabolism. They suggest a novel role for mitochondria in cartilage homeostasis that is independent of oxidative phosphorylation.</description><identifier>ISSN: 1063-4584</identifier><identifier>EISSN: 1522-9653</identifier><identifier>DOI: 10.1016/j.joca.2012.01.003</identifier><identifier>PMID: 22305999</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Adenosine triphosphate ; Adenosine Triphosphate - biosynthesis ; Animals ; Cartilage ; Cartilage, Articular - metabolism ; Cattle ; Chondrocytes - metabolism ; Electron Transport - drug effects ; Electron Transport - physiology ; Fluorodeoxyglucose F18 - pharmacology ; Glycolysis ; Glycolysis - drug effects ; Glycolysis - physiology ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mitochondrial electron transport ; Oxidants ; Rheumatology ; Rotenone - pharmacology ; Superoxides - metabolism ; Tissue Culture Techniques ; Uncoupling Agents - pharmacology</subject><ispartof>Osteoarthritis and cartilage, 2012-04, Vol.20 (4), p.323-329</ispartof><rights>Osteoarthritis Research Society International</rights><rights>2012 Osteoarthritis Research Society International</rights><rights>Copyright © 2012 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.</rights><rights>2012 OsteoArthritis Society International. Published by Elsevier Ltd. All rights reserved. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-a5dd2ab938e6ab7c6390fe263232007bdad35423fe3b174e98c58d10c73208f13</citedby><cites>FETCH-LOGICAL-c509t-a5dd2ab938e6ab7c6390fe263232007bdad35423fe3b174e98c58d10c73208f13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1063458412000246$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22305999$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Martin, J.A</creatorcontrib><creatorcontrib>Martini, A</creatorcontrib><creatorcontrib>Molinari, A</creatorcontrib><creatorcontrib>Morgan, W</creatorcontrib><creatorcontrib>Ramalingam, W</creatorcontrib><creatorcontrib>Buckwalter, J.A</creatorcontrib><creatorcontrib>McKinley, T.O</creatorcontrib><title>Mitochondrial electron transport and glycolysis are coupled in articular cartilage</title><title>Osteoarthritis and cartilage</title><addtitle>Osteoarthritis Cartilage</addtitle><description>Summary Objective Although the majority of the adenosine triphosphate (ATP) in chondrocytes is made by glycolysis rather than by oxidative phosphorylation in mitochondria there is evidence to suggest that reactive oxygen species produced by mitochondrial electron transport (ET) help to maintain cellular redox balance in favor of glycolysis. The objective of this study was to test this hypothesis by determining if rotenone, which inhibits ET and blocks oxidant production inhibits glycolytic ATP synthesis. Design Bovine osteochondral explants were treated with rotenone, an ET inhibitor; or oligomycin an ATP synthase inhibitor; or 2-fluoro-2-deoxy- d -glucose, a glycolysis inhibiter; or peroxide, an exogenous oxidant; or mitoquinone (MitoQ), a mitochondria-targeted anti-oxidant. Cartilage extracts were assayed for ATP, nicotine adenine dinucleotide (NAD+/H), and culture medium was assayed for pyruvate and lactate after 24 h of treatment. Imaging studies were used to measure superoxide production in cartilage. Results Rotenone and 2-FG caused a significant decline in cartilage ATP ( P < 0.001). In contrast, ATP levels were not affected by oligomycin. Peroxide treatment blocked rotenone effects on ATP, while treatment with MitoQ significantly suppressed ATP levels. Rotenone and 2-FG caused a significant decline in pyruvate, but not in lactate production. NADH:NAD+ ratios decreased significantly in both rotenone and 2-FG-treated explants ( P < 0.05). Rotenone also significantly reduced superoxide production. Conclusions These findings showing a link between glycolysis and ET are consistent with previous reports on the critical need for oxidants to support normal chondrocyte metabolism. They suggest a novel role for mitochondria in cartilage homeostasis that is independent of oxidative phosphorylation.</description><subject>Adenosine triphosphate</subject><subject>Adenosine Triphosphate - biosynthesis</subject><subject>Animals</subject><subject>Cartilage</subject><subject>Cartilage, Articular - metabolism</subject><subject>Cattle</subject><subject>Chondrocytes - metabolism</subject><subject>Electron Transport - drug effects</subject><subject>Electron Transport - physiology</subject><subject>Fluorodeoxyglucose F18 - pharmacology</subject><subject>Glycolysis</subject><subject>Glycolysis - drug effects</subject><subject>Glycolysis - physiology</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondrial electron transport</subject><subject>Oxidants</subject><subject>Rheumatology</subject><subject>Rotenone - pharmacology</subject><subject>Superoxides - metabolism</subject><subject>Tissue Culture Techniques</subject><subject>Uncoupling Agents - pharmacology</subject><issn>1063-4584</issn><issn>1522-9653</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kdFq3DAQRUVpaNK0P9CH4B-wO5Jsrw0lUELSFhICafMs5NF4I0eRFsm7sH8fmU1D24c-acTce0c6w9gnDhUH3n6eqimgrgRwUQGvAOQbdsIbIcq-beTbXEMry7rp6mP2PqUJsoJzeMeOhZDQ9H1_wu5u7BzwIXgTrXYFOcI5Bl_MUfu0CXEutDfF2u0xuH2yqdCRCgzbjSNTWJ-vs8Wt07HApXR6TR_Y0ahdoo8v5ym7v7r8dfG9vL799uPi63WJDfRzqRtjhB562VGrhxW2soeRRCuFFACrwWgjm1rIkeTAVzX1HTad4YCr3O9GLk_Z-SF3sx2eyCD5_GinNtE-6bhXQVv1d8fbB7UOOyVbWUvR5QBxCMAYUoo0vno5qIWwmtRCWC2EFXCV-WXT2Z9TXy2_kWbBl4OA8t93lqJKaMkjGRszXGWC_X_--T92dNZb1O6R9pSmsI0-U1VcpexRP5cdLyvmGRqIupXPma2kDA</recordid><startdate>20120401</startdate><enddate>20120401</enddate><creator>Martin, J.A</creator><creator>Martini, A</creator><creator>Molinari, A</creator><creator>Morgan, W</creator><creator>Ramalingam, W</creator><creator>Buckwalter, J.A</creator><creator>McKinley, T.O</creator><general>Elsevier Ltd</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>20120401</creationdate><title>Mitochondrial electron transport and glycolysis are coupled in articular cartilage</title><author>Martin, J.A ; Martini, A ; Molinari, A ; Morgan, W ; Ramalingam, W ; Buckwalter, J.A ; McKinley, T.O</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-a5dd2ab938e6ab7c6390fe263232007bdad35423fe3b174e98c58d10c73208f13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adenosine triphosphate</topic><topic>Adenosine Triphosphate - biosynthesis</topic><topic>Animals</topic><topic>Cartilage</topic><topic>Cartilage, Articular - metabolism</topic><topic>Cattle</topic><topic>Chondrocytes - metabolism</topic><topic>Electron Transport - drug effects</topic><topic>Electron Transport - physiology</topic><topic>Fluorodeoxyglucose F18 - pharmacology</topic><topic>Glycolysis</topic><topic>Glycolysis - drug effects</topic><topic>Glycolysis - physiology</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondrial electron transport</topic><topic>Oxidants</topic><topic>Rheumatology</topic><topic>Rotenone - pharmacology</topic><topic>Superoxides - metabolism</topic><topic>Tissue Culture Techniques</topic><topic>Uncoupling Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Martin, J.A</creatorcontrib><creatorcontrib>Martini, A</creatorcontrib><creatorcontrib>Molinari, A</creatorcontrib><creatorcontrib>Morgan, W</creatorcontrib><creatorcontrib>Ramalingam, W</creatorcontrib><creatorcontrib>Buckwalter, J.A</creatorcontrib><creatorcontrib>McKinley, T.O</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Osteoarthritis and cartilage</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martin, J.A</au><au>Martini, A</au><au>Molinari, A</au><au>Morgan, W</au><au>Ramalingam, W</au><au>Buckwalter, J.A</au><au>McKinley, T.O</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondrial electron transport and glycolysis are coupled in articular cartilage</atitle><jtitle>Osteoarthritis and cartilage</jtitle><addtitle>Osteoarthritis Cartilage</addtitle><date>2012-04-01</date><risdate>2012</risdate><volume>20</volume><issue>4</issue><spage>323</spage><epage>329</epage><pages>323-329</pages><issn>1063-4584</issn><eissn>1522-9653</eissn><abstract>Summary Objective Although the majority of the adenosine triphosphate (ATP) in chondrocytes is made by glycolysis rather than by oxidative phosphorylation in mitochondria there is evidence to suggest that reactive oxygen species produced by mitochondrial electron transport (ET) help to maintain cellular redox balance in favor of glycolysis. The objective of this study was to test this hypothesis by determining if rotenone, which inhibits ET and blocks oxidant production inhibits glycolytic ATP synthesis. Design Bovine osteochondral explants were treated with rotenone, an ET inhibitor; or oligomycin an ATP synthase inhibitor; or 2-fluoro-2-deoxy- d -glucose, a glycolysis inhibiter; or peroxide, an exogenous oxidant; or mitoquinone (MitoQ), a mitochondria-targeted anti-oxidant. Cartilage extracts were assayed for ATP, nicotine adenine dinucleotide (NAD+/H), and culture medium was assayed for pyruvate and lactate after 24 h of treatment. Imaging studies were used to measure superoxide production in cartilage. Results Rotenone and 2-FG caused a significant decline in cartilage ATP ( P < 0.001). In contrast, ATP levels were not affected by oligomycin. Peroxide treatment blocked rotenone effects on ATP, while treatment with MitoQ significantly suppressed ATP levels. Rotenone and 2-FG caused a significant decline in pyruvate, but not in lactate production. NADH:NAD+ ratios decreased significantly in both rotenone and 2-FG-treated explants ( P < 0.05). Rotenone also significantly reduced superoxide production. Conclusions These findings showing a link between glycolysis and ET are consistent with previous reports on the critical need for oxidants to support normal chondrocyte metabolism. They suggest a novel role for mitochondria in cartilage homeostasis that is independent of oxidative phosphorylation.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>22305999</pmid><doi>10.1016/j.joca.2012.01.003</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenosine triphosphate Adenosine Triphosphate - biosynthesis Animals Cartilage Cartilage, Articular - metabolism Cattle Chondrocytes - metabolism Electron Transport - drug effects Electron Transport - physiology Fluorodeoxyglucose F18 - pharmacology Glycolysis Glycolysis - drug effects Glycolysis - physiology Mitochondria - drug effects Mitochondria - metabolism Mitochondrial electron transport Oxidants Rheumatology Rotenone - pharmacology Superoxides - metabolism Tissue Culture Techniques Uncoupling Agents - pharmacology |
| title | Mitochondrial electron transport and glycolysis are coupled in articular cartilage |
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