Cross talk between NADPH oxidase and autophagy in pulmonary artery endothelial cells with intrauterine persistent pulmonary hypertension
Identifieur interne : 001454 ( Main/Exploration ); précédent : 001453; suivant : 001455Cross talk between NADPH oxidase and autophagy in pulmonary artery endothelial cells with intrauterine persistent pulmonary hypertension
Auteurs : Ru-Jeng Teng [États-Unis] ; JIANHAI DU [États-Unis] ; Scott Welak [États-Unis] ; TONGJU GUAN [États-Unis] ; Annie Eis [États-Unis] ; YANG SHI [États-Unis] ; Girija G. Konduri [États-Unis]Source :
- American journal of physiology. Lung cellular and molecular physiology [ 1040-0605 ] ; 2012.
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Abstract
Autophagy is a process for cells to degrade proteins or entire organelles to maintain a balance in the synthesis, degradation, and subsequent recycling of cellular products. Increased reactive oxygen species formation is known to induce autophagy. We previously reported that increased NADPH oxidase (NOX) activity in pulmonary artery endothelial cells (PAEC) from fetal lambs with persistent pulmonary hypertension (PPHN) contributes to impaired angiogenesis in PPHN-PAEC compared with normal PAEC. We hypothesized that increased NOX activity in PPHN-PAEC is associated with increased autophagy, which, in turn, contributes to impaired angiogenesis in PPHN-PAEC. In the present study, we detected increased autophagy in PPHN-PAEC as shown by increased ratio of the microtubule-associated protein 1 light chain (LC3)-II to LC3-I and increased percentage of green fluorescent protein-LC3 punctate positive cells. Inhibiting autophagy by 3-methyladenine, chloroquine, and beclin-1 knockdown in PPHN-PAEC has led to decreased autophagy and increased in vitro angiogenesis. Inhibition of autophagy also decreased the association between gp91phox and p47phox, NOX activity, and superoxide generation. A nonspecific antioxidant N-acetylcysteine and a NOX inhibitor apocynin decreased autophagy in PPHN-PAEC. In conclusion, autophagy may contribute to impaired angiogenesis in PPHN-PAEC through increasing NOX activity. Our results suggest that, in PPHN-PAEC, a positive feedback relationship between autophagy and NOX activity may regulate angiogenesis.
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Konduri</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Division of Neonatology, Department of Pediatrics, Medical College of Wisconsin</s1><s2>Wauwatosa, Wisconsin</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Wisconsin</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">12-0245190</idno><date when="2012">2012</date><idno type="stanalyst">PASCAL 12-0245190 INIST</idno><idno type="RBID">Pascal:12-0245190</idno><idno type="wicri:Area/PascalFrancis/Corpus">000010</idno><idno type="wicri:Area/PascalFrancis/Curation">000056</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000012</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000012</idno><idno type="wicri:doubleKey">1040-0605:2012:Teng R:cross:talk:between</idno><idno type="wicri:Area/Main/Merge">001456</idno><idno type="wicri:Area/Main/Curation">001454</idno><idno type="wicri:Area/Main/Exploration">001454</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Cross talk between NADPH oxidase and autophagy in pulmonary artery endothelial cells with intrauterine persistent pulmonary hypertension</title><author><name sortKey="Teng, Ru Jeng" sort="Teng, Ru Jeng" uniqKey="Teng R" first="Ru-Jeng" last="Teng">Ru-Jeng Teng</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Division of Neonatology, Department of Pediatrics, Medical College of Wisconsin</s1><s2>Wauwatosa, Wisconsin</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Wisconsin</region></placeName></affiliation></author><author><name sortKey="Jianhai Du" sort="Jianhai Du" uniqKey="Jianhai Du" last="Jianhai Du">JIANHAI DU</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Division of Pediatric Surgery, Department of Surgery, Medical College of Wisconsin</s1><s2>Wauwatosa, Wisconsin</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Wisconsin</region></placeName></affiliation></author><author><name sortKey="Welak, Scott" sort="Welak, Scott" uniqKey="Welak S" first="Scott" last="Welak">Scott Welak</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Division of Neonatology, Department of Pediatrics, Medical College of Wisconsin</s1><s2>Wauwatosa, Wisconsin</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Wisconsin</region></placeName></affiliation></author><author><name sortKey="Tongju Guan" sort="Tongju Guan" uniqKey="Tongju Guan" last="Tongju Guan">TONGJU GUAN</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Division of Pediatric Surgery, Department of Surgery, Medical College of Wisconsin</s1><s2>Wauwatosa, Wisconsin</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Wisconsin</region></placeName></affiliation></author><author><name sortKey="Eis, Annie" sort="Eis, Annie" uniqKey="Eis A" first="Annie" last="Eis">Annie Eis</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Division of Neonatology, Department of Pediatrics, Medical College of Wisconsin</s1><s2>Wauwatosa, Wisconsin</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Wisconsin</region></placeName></affiliation></author><author><name sortKey="Yang Shi" sort="Yang Shi" uniqKey="Yang Shi" last="Yang Shi">YANG SHI</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Division of Pediatric Surgery, Department of Surgery, Medical College of Wisconsin</s1><s2>Wauwatosa, Wisconsin</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Wisconsin</region></placeName></affiliation></author><author><name sortKey="Konduri, Girija G" sort="Konduri, Girija G" uniqKey="Konduri G" first="Girija G." last="Konduri">Girija G. Konduri</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Division of Neonatology, Department of Pediatrics, Medical College of Wisconsin</s1><s2>Wauwatosa, Wisconsin</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Wisconsin</region></placeName></affiliation></author></analytic><series><title level="j" type="main">American journal of physiology. Lung cellular and molecular physiology</title><title level="j" type="abbreviated">Am. j. physiol., Lung cell. mol. physiol.</title><idno type="ISSN">1040-0605</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">American journal of physiology. Lung cellular and molecular physiology</title><title level="j" type="abbreviated">Am. j. physiol., Lung cell. mol. physiol.</title><idno type="ISSN">1040-0605</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Endothelial cell</term><term>Mammalia</term><term>Oxidase</term><term>Pulmonary artery</term><term>Pulmonary hypertension</term><term>Respiratory system</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Oxidase</term><term>Artère pulmonaire</term><term>Cellule endothéliale</term><term>Hypertension artérielle pulmonaire</term><term>Mammalia</term><term>Appareil respiratoire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Autophagy is a process for cells to degrade proteins or entire organelles to maintain a balance in the synthesis, degradation, and subsequent recycling of cellular products. Increased reactive oxygen species formation is known to induce autophagy. We previously reported that increased NADPH oxidase (NOX) activity in pulmonary artery endothelial cells (PAEC) from fetal lambs with persistent pulmonary hypertension (PPHN) contributes to impaired angiogenesis in PPHN-PAEC compared with normal PAEC. We hypothesized that increased NOX activity in PPHN-PAEC is associated with increased autophagy, which, in turn, contributes to impaired angiogenesis in PPHN-PAEC. In the present study, we detected increased autophagy in PPHN-PAEC as shown by increased ratio of the microtubule-associated protein 1 light chain (LC3)-II to LC3-I and increased percentage of green fluorescent protein-LC3 punctate positive cells. Inhibiting autophagy by 3-methyladenine, chloroquine, and beclin-1 knockdown in PPHN-PAEC has led to decreased autophagy and increased in vitro angiogenesis. Inhibition of autophagy also decreased the association between gp91<sup>phox</sup> and p47<sup>phox</sup>, NOX activity, and superoxide generation. A nonspecific antioxidant N-acetylcysteine and a NOX inhibitor apocynin decreased autophagy in PPHN-PAEC. In conclusion, autophagy may contribute to impaired angiogenesis in PPHN-PAEC through increasing NOX activity. Our results suggest that, in PPHN-PAEC, a positive feedback relationship between autophagy and NOX activity may regulate angiogenesis.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Wisconsin</li></region></list><tree><country name="États-Unis"><region name="Wisconsin"><name sortKey="Teng, Ru Jeng" sort="Teng, Ru Jeng" uniqKey="Teng R" first="Ru-Jeng" last="Teng">Ru-Jeng Teng</name></region><name sortKey="Eis, Annie" sort="Eis, Annie" uniqKey="Eis A" first="Annie" last="Eis">Annie Eis</name><name sortKey="Jianhai Du" sort="Jianhai Du" uniqKey="Jianhai Du" last="Jianhai Du">JIANHAI DU</name><name sortKey="Konduri, Girija G" sort="Konduri, Girija G" uniqKey="Konduri G" first="Girija G." last="Konduri">Girija G. Konduri</name><name sortKey="Tongju Guan" sort="Tongju Guan" uniqKey="Tongju Guan" last="Tongju Guan">TONGJU GUAN</name><name sortKey="Welak, Scott" sort="Welak, Scott" uniqKey="Welak S" first="Scott" last="Welak">Scott Welak</name><name sortKey="Yang Shi" sort="Yang Shi" uniqKey="Yang Shi" last="Yang Shi">YANG SHI</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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