Mitochondrial Oxidative Stress Corrupts Coronary Collateral Growth by Activating Adenosine Monophosphate Activated Kinase-α Signaling
Identifieur interne : 000889 ( Pmc/Curation ); précédent : 000888; suivant : 000890Mitochondrial Oxidative Stress Corrupts Coronary Collateral Growth by Activating Adenosine Monophosphate Activated Kinase-α Signaling
Auteurs : Yuh Fen Pung ; Wai Johnn Sam ; Kelly Stevanov ; Molly Enrick ; Chwen-Lih Chen ; Christopher Kolz ; Prashanth Thakker ; James P. Hardwick ; Yeong-Renn Chen ; Jason R. B. Dyck ; Liya Yin ; William M. ChilianSource :
- Arteriosclerosis, thrombosis, and vascular biology [ 1079-5642 ] ; 2013.
Abstract
Our goal was to determine the mechanism by which mitochondrial oxidative stress impairs collateral growth in the heart.
Rats were treated with rotenone (mitochondrial complex I inhibitor that increases reactive oxygen species production) or sham-treated with vehicle and subjected to repetitive ischemia protocol for 10 days to induce coronary collateral growth. In control rats, repetitive ischemia increased flow to the collateral-dependent zone; however, rotenone treatment prevented this increase suggesting that mitochondrial oxidative stress compromises coronary collateral growth. In addition, rotenone also attenuated mitochondrial complex I activity and led to excessive mitochondrial aggregation. To further understand the mechanistic pathway(s) involved, human coronary artery endothelial cells were treated with 50 ng/ mL vascular endothelial growth factor, 1 µmol/L rotenone, and rotenone/vascular endothelial growth factor for 48 hours. Vascular endothelial growth factor induced robust tube formation; however, rotenone completely inhibited this effect (
We conclude that activation of AMPK-α during mitochondrial oxidative stress inhibits mammalian target of rapamycin signaling, which impairs phenotypic switching necessary for the growth of blood vessels.
Url:
DOI: 10.1161/ATVBAHA.113.301591
PubMed: 23788766
PubMed Central: 4402936
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<author><name sortKey="Pung, Yuh Fen" sort="Pung, Yuh Fen" uniqKey="Pung Y" first="Yuh Fen" last="Pung">Yuh Fen Pung</name>
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<author><name sortKey="Sam, Wai Johnn" sort="Sam, Wai Johnn" uniqKey="Sam W" first="Wai Johnn" last="Sam">Wai Johnn Sam</name>
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<author><name sortKey="Stevanov, Kelly" sort="Stevanov, Kelly" uniqKey="Stevanov K" first="Kelly" last="Stevanov">Kelly Stevanov</name>
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<author><name sortKey="Enrick, Molly" sort="Enrick, Molly" uniqKey="Enrick M" first="Molly" last="Enrick">Molly Enrick</name>
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<author><name sortKey="Chen, Chwen Lih" sort="Chen, Chwen Lih" uniqKey="Chen C" first="Chwen-Lih" last="Chen">Chwen-Lih Chen</name>
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<author><name sortKey="Kolz, Christopher" sort="Kolz, Christopher" uniqKey="Kolz C" first="Christopher" last="Kolz">Christopher Kolz</name>
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<author><name sortKey="Pung, Yuh Fen" sort="Pung, Yuh Fen" uniqKey="Pung Y" first="Yuh Fen" last="Pung">Yuh Fen Pung</name>
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<author><name sortKey="Sam, Wai Johnn" sort="Sam, Wai Johnn" uniqKey="Sam W" first="Wai Johnn" last="Sam">Wai Johnn Sam</name>
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<author><name sortKey="Enrick, Molly" sort="Enrick, Molly" uniqKey="Enrick M" first="Molly" last="Enrick">Molly Enrick</name>
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<author><name sortKey="Chen, Chwen Lih" sort="Chen, Chwen Lih" uniqKey="Chen C" first="Chwen-Lih" last="Chen">Chwen-Lih Chen</name>
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<author><name sortKey="Kolz, Christopher" sort="Kolz, Christopher" uniqKey="Kolz C" first="Christopher" last="Kolz">Christopher Kolz</name>
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<series><title level="j">Arteriosclerosis, thrombosis, and vascular biology</title>
<idno type="ISSN">1079-5642</idno>
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Objective</title>
<p id="P1">Our goal was to determine the mechanism by which mitochondrial oxidative stress impairs collateral growth in the heart.</p>
</sec>
<sec id="S2"><title>Approach and Results</title>
<p id="P2">Rats were treated with rotenone (mitochondrial complex I inhibitor that increases reactive oxygen species production) or sham-treated with vehicle and subjected to repetitive ischemia protocol for 10 days to induce coronary collateral growth. In control rats, repetitive ischemia increased flow to the collateral-dependent zone; however, rotenone treatment prevented this increase suggesting that mitochondrial oxidative stress compromises coronary collateral growth. In addition, rotenone also attenuated mitochondrial complex I activity and led to excessive mitochondrial aggregation. To further understand the mechanistic pathway(s) involved, human coronary artery endothelial cells were treated with 50 ng/ mL vascular endothelial growth factor, 1 µmol/L rotenone, and rotenone/vascular endothelial growth factor for 48 hours. Vascular endothelial growth factor induced robust tube formation; however, rotenone completely inhibited this effect (<italic>P</italic>
<0.05 rotenone versus vascular endothelial growth factor treatment). Inhibition of tube formation by rotenone was also associated with significant increase in mitochondrial superoxide generation. Immunoblot analyses of human coronary artery endothelial cells with rotenone treatment showed significant activation of adenosine monophosphate activated kinase (AMPK)-α and inhibition of mammalian target of rapamycin and p70 ribosomal S6 kinase. Activation of AMPK-α suggested impairments in energy production, which was reflected by decrease in O<sub>2</sub>
consumption and bioenergetic reserve capacity of cultured cells. Knockdown of AMPK-α (siRNA) also preserved tube formation during rotenone, suggesting the negative effects were mediated by the activation of AMPK-α. Conversely, expression of a constitutively active AMPK-α blocked tube formation.</p>
</sec>
<sec id="S3"><title>Conclusions</title>
<p id="P3">We conclude that activation of AMPK-α during mitochondrial oxidative stress inhibits mammalian target of rapamycin signaling, which impairs phenotypic switching necessary for the growth of blood vessels.</p>
</sec>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">9505803</journal-id>
<journal-id journal-id-type="pubmed-jr-id">8623</journal-id>
<journal-id journal-id-type="nlm-ta">Arterioscler Thromb Vasc Biol</journal-id>
<journal-id journal-id-type="iso-abbrev">Arterioscler. Thromb. Vasc. Biol.</journal-id>
<journal-title-group><journal-title>Arteriosclerosis, thrombosis, and vascular biology</journal-title>
</journal-title-group>
<issn pub-type="ppub">1079-5642</issn>
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<article-id pub-id-type="pmc">4402936</article-id>
<article-id pub-id-type="doi">10.1161/ATVBAHA.113.301591</article-id>
<article-id pub-id-type="manuscript">NIHMS572238</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
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<title-group><article-title>Mitochondrial Oxidative Stress Corrupts Coronary Collateral Growth by Activating Adenosine Monophosphate Activated Kinase-α Signaling</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Pung</surname>
<given-names>Yuh Fen</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Sam</surname>
<given-names>Wai Johnn</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Stevanov</surname>
<given-names>Kelly</given-names>
</name>
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<contrib contrib-type="author"><name><surname>Enrick</surname>
<given-names>Molly</given-names>
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<contrib contrib-type="author"><name><surname>Chen</surname>
<given-names>Chwen-Lih</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Kolz</surname>
<given-names>Christopher</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Thakker</surname>
<given-names>Prashanth</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Hardwick</surname>
<given-names>James P.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Chen</surname>
<given-names>Yeong-Renn</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Dyck</surname>
<given-names>Jason R.B.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Yin</surname>
<given-names>Liya</given-names>
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<contrib contrib-type="author"><name><surname>Chilian</surname>
<given-names>William M.</given-names>
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<aff id="A1">Department of Integrative Medical Sciences, Northeast Ohio Medical University, Rootstown, OH (Y.F.P., W.J.S., K.S., M.E., C.-L.C., C.K., P.T., J.P.H., Y.-R.C., L.Y., W.M.C.); and Department of Pediatrics, Faculty of Medicine and Dentistry, Cardiovascular Research Centre, University of Alberta, Edmonton, Canada (J.R.B.D.)</aff>
</contrib-group>
<author-notes><corresp id="cor1">Correspondence to William M. Chilian, PhD, Department of Integrative Medical Sciences, Northeast Ohio Medical University, Rootstown, OH 44272. <email>wchilian@neomed.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>14</day>
<month>4</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="epub"><day>20</day>
<month>6</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="ppub"><month>8</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>20</day>
<month>4</month>
<year>2015</year>
</pub-date>
<volume>33</volume>
<issue>8</issue>
<fpage>1911</fpage>
<lpage>1919</lpage>
<pmc-comment>elocation-id from pubmed: 10.1161/ATVBAHA.113.301591</pmc-comment>
<permissions><copyright-statement>© 2013 American Heart Association, Inc.</copyright-statement>
<copyright-year>2013</copyright-year>
</permissions>
<abstract><sec id="S1"><title>Objective</title>
<p id="P1">Our goal was to determine the mechanism by which mitochondrial oxidative stress impairs collateral growth in the heart.</p>
</sec>
<sec id="S2"><title>Approach and Results</title>
<p id="P2">Rats were treated with rotenone (mitochondrial complex I inhibitor that increases reactive oxygen species production) or sham-treated with vehicle and subjected to repetitive ischemia protocol for 10 days to induce coronary collateral growth. In control rats, repetitive ischemia increased flow to the collateral-dependent zone; however, rotenone treatment prevented this increase suggesting that mitochondrial oxidative stress compromises coronary collateral growth. In addition, rotenone also attenuated mitochondrial complex I activity and led to excessive mitochondrial aggregation. To further understand the mechanistic pathway(s) involved, human coronary artery endothelial cells were treated with 50 ng/ mL vascular endothelial growth factor, 1 µmol/L rotenone, and rotenone/vascular endothelial growth factor for 48 hours. Vascular endothelial growth factor induced robust tube formation; however, rotenone completely inhibited this effect (<italic>P</italic>
<0.05 rotenone versus vascular endothelial growth factor treatment). Inhibition of tube formation by rotenone was also associated with significant increase in mitochondrial superoxide generation. Immunoblot analyses of human coronary artery endothelial cells with rotenone treatment showed significant activation of adenosine monophosphate activated kinase (AMPK)-α and inhibition of mammalian target of rapamycin and p70 ribosomal S6 kinase. Activation of AMPK-α suggested impairments in energy production, which was reflected by decrease in O<sub>2</sub>
consumption and bioenergetic reserve capacity of cultured cells. Knockdown of AMPK-α (siRNA) also preserved tube formation during rotenone, suggesting the negative effects were mediated by the activation of AMPK-α. Conversely, expression of a constitutively active AMPK-α blocked tube formation.</p>
</sec>
<sec id="S3"><title>Conclusions</title>
<p id="P3">We conclude that activation of AMPK-α during mitochondrial oxidative stress inhibits mammalian target of rapamycin signaling, which impairs phenotypic switching necessary for the growth of blood vessels.</p>
</sec>
</abstract>
<kwd-group><kwd>collateral circulation</kwd>
<kwd>coronary circulation</kwd>
<kwd>mitochondria</kwd>
<kwd>reactive oxygen species</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
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