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Article: Inhibition of protein kinase C β 2 prevents tumor necrosis factor-α-induced apoptosis and oxidative stress in endothelial cells: The role of NADPH oxidase subunits
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TitleInhibition of protein kinase C β 2 prevents tumor necrosis factor-α-induced apoptosis and oxidative stress in endothelial cells: The role of NADPH oxidase subunits
 
AuthorsDeng, B2
Xie, S2
Wang, J2
Xia, Z1
Nie, R2
 
KeywordsApoptosis
Human Umbilical Vein Endothelial Cells
Nadph Oxidase
Protein Kinase C Β 2
Reactive Oxygen Species
 
Issue Date2012
 
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR
 
CitationJournal Of Vascular Research, 2012, v. 49 n. 2, p. 144-159 [How to Cite?]
DOI: http://dx.doi.org/10.1159/000332337
 
AbstractWe investigate the cell signal transduction pathway protein kinase C (PKC) and the role of NADPH subunits in the process of TNF-α-induced endothelial apoptosis. Human umbilical vein endothelial cells (HUVEC) were treated with one of these: 1 mM PKC β 2 inhibitor CGP53353, 10 mM PKC δ inhibitor rottlerin, combination CGP53353 with rottlerin, 3 ×10 -4M NADPH oxidase inhibitor apocynin, 5 × 10 -6M NADPH oxidase peptide inhibitor gp91ds-tat. The apoptosis process was assessed by Hoechst 33342 stain, flow cytometry and Western blot analysis, while intracellular reactive oxygen species (ROS) production was detected by 2,7'-dichlorodihydrofluorescein diacetate (DCFH-DA). The NADPH oxidase subunit gene and protein expression were assessed by quantitative real-time PCR and Western blot analysis, respectively. TNF-α significantly induced HUVEC apoptosis and ROS production, accompanying with dramatic upregulation of NADPH oxidase subunits: NOX2/gp91 phox, NOX4, p47 phox and p67 phox, whereas these enhancements were abolished by the treatment with PKC inhibitors. High TNF-α level exposure induces HUVEC apoptosis, as well as a ROS generation increase via the PKC β 2-dependent activation of NADPH oxidase. Although the PKC δ pathway may enhance TNF-α-induced HUVEC apoptosis, it does not involve the ROS pathway. Upregulation of expression of NADPH subunits is important in this process, which leads to a new target in antioxidative therapy for vascular disease prevention. Copyright © 2012 S. Karger AG.
 
ISSN1018-1172
2012 Impact Factor: 2.434
2012 SCImago Journal Rankings: 0.876
 
DOIhttp://dx.doi.org/10.1159/000332337
 
ISI Accession Number IDWOS:000303152300006
Funding AgencyGrant Number
National Nature Science Foundation of China30770899
Nature Science Foundation of Guangdong province of China815100890100072
Funding Information:

We are grateful to Professor Rui Zhang (Department of Maternity, Sun Yat-Sen Memorial Hospital, Sun Yet-Sen University) for her helpful assistance, and to Dr. Huimin Liu (Anesthesiology Research Laboratory, Renmin Hospital, Wuhan University) for scientific advice. This work was supported in part by grants from the National Nature Science Foundation of China (No. 30770899 to R.N.) and the Nature Science Foundation of Guangdong province of China (No. 815100890100072 to R.N.).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorDeng, B
 
dc.contributor.authorXie, S
 
dc.contributor.authorWang, J
 
dc.contributor.authorXia, Z
 
dc.contributor.authorNie, R
 
dc.date.accessioned2012-05-29T06:01:15Z
 
dc.date.available2012-05-29T06:01:15Z
 
dc.date.issued2012
 
dc.description.abstractWe investigate the cell signal transduction pathway protein kinase C (PKC) and the role of NADPH subunits in the process of TNF-α-induced endothelial apoptosis. Human umbilical vein endothelial cells (HUVEC) were treated with one of these: 1 mM PKC β 2 inhibitor CGP53353, 10 mM PKC δ inhibitor rottlerin, combination CGP53353 with rottlerin, 3 ×10 -4M NADPH oxidase inhibitor apocynin, 5 × 10 -6M NADPH oxidase peptide inhibitor gp91ds-tat. The apoptosis process was assessed by Hoechst 33342 stain, flow cytometry and Western blot analysis, while intracellular reactive oxygen species (ROS) production was detected by 2,7'-dichlorodihydrofluorescein diacetate (DCFH-DA). The NADPH oxidase subunit gene and protein expression were assessed by quantitative real-time PCR and Western blot analysis, respectively. TNF-α significantly induced HUVEC apoptosis and ROS production, accompanying with dramatic upregulation of NADPH oxidase subunits: NOX2/gp91 phox, NOX4, p47 phox and p67 phox, whereas these enhancements were abolished by the treatment with PKC inhibitors. High TNF-α level exposure induces HUVEC apoptosis, as well as a ROS generation increase via the PKC β 2-dependent activation of NADPH oxidase. Although the PKC δ pathway may enhance TNF-α-induced HUVEC apoptosis, it does not involve the ROS pathway. Upregulation of expression of NADPH subunits is important in this process, which leads to a new target in antioxidative therapy for vascular disease prevention. Copyright © 2012 S. Karger AG.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationJournal Of Vascular Research, 2012, v. 49 n. 2, p. 144-159 [How to Cite?]
DOI: http://dx.doi.org/10.1159/000332337
 
dc.identifier.doihttp://dx.doi.org/10.1159/000332337
 
dc.identifier.epage159
 
dc.identifier.isiWOS:000303152300006
Funding AgencyGrant Number
National Nature Science Foundation of China30770899
Nature Science Foundation of Guangdong province of China815100890100072
Funding Information:

We are grateful to Professor Rui Zhang (Department of Maternity, Sun Yat-Sen Memorial Hospital, Sun Yet-Sen University) for her helpful assistance, and to Dr. Huimin Liu (Anesthesiology Research Laboratory, Renmin Hospital, Wuhan University) for scientific advice. This work was supported in part by grants from the National Nature Science Foundation of China (No. 30770899 to R.N.) and the Nature Science Foundation of Guangdong province of China (No. 815100890100072 to R.N.).

 
dc.identifier.issn1018-1172
2012 Impact Factor: 2.434
2012 SCImago Journal Rankings: 0.876
 
dc.identifier.issue2
 
dc.identifier.pmid22261918
 
dc.identifier.scopuseid_2-s2.0-84862811283
 
dc.identifier.spage144
 
dc.identifier.urihttp://hdl.handle.net/10722/147287
 
dc.identifier.volume49
 
dc.languageeng
 
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR
 
dc.publisher.placeSwitzerland
 
dc.relation.ispartofJournal of Vascular Research
 
dc.relation.referencesReferences in Scopus
 
dc.subjectApoptosis
 
dc.subjectHuman Umbilical Vein Endothelial Cells
 
dc.subjectNadph Oxidase
 
dc.subjectProtein Kinase C Β 2
 
dc.subjectReactive Oxygen Species
 
dc.titleInhibition of protein kinase C β 2 prevents tumor necrosis factor-α-induced apoptosis and oxidative stress in endothelial cells: The role of NADPH oxidase subunits
 
dc.typeArticle
 
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<contributor.author>Nie, R</contributor.author>
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<description.abstract>We investigate the cell signal transduction pathway protein kinase C (PKC) and the role of NADPH subunits in the process of TNF-&#945;-induced endothelial apoptosis. Human umbilical vein endothelial cells (HUVEC) were treated with one of these: 1 mM PKC &#946; 2 inhibitor CGP53353, 10 mM PKC &#948; inhibitor rottlerin, combination CGP53353 with rottlerin, 3 &#215;10 -4M NADPH oxidase inhibitor apocynin, 5 &#215; 10 -6M NADPH oxidase peptide inhibitor gp91ds-tat. The apoptosis process was assessed by Hoechst 33342 stain, flow cytometry and Western blot analysis, while intracellular reactive oxygen species (ROS) production was detected by 2,7&apos;-dichlorodihydrofluorescein diacetate (DCFH-DA). The NADPH oxidase subunit gene and protein expression were assessed by quantitative real-time PCR and Western blot analysis, respectively. TNF-&#945; significantly induced HUVEC apoptosis and ROS production, accompanying with dramatic upregulation of NADPH oxidase subunits: NOX2/gp91 phox, NOX4, p47 phox and p67 phox, whereas these enhancements were abolished by the treatment with PKC inhibitors. High TNF-&#945; level exposure induces HUVEC apoptosis, as well as a ROS generation increase via the PKC &#946; 2-dependent activation of NADPH oxidase. Although the PKC &#948; pathway may enhance TNF-&#945;-induced HUVEC apoptosis, it does not involve the ROS pathway. Upregulation of expression of NADPH subunits is important in this process, which leads to a new target in antioxidative therapy for vascular disease prevention. Copyright &#169; 2012 S. Karger AG.</description.abstract>
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Author Affiliations
  1. Hubei General Hospital
  2. Sun Yat-Sen University