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Vascular endothelial growth factor as an autocrine survival factor for retinal pigment epithelial cells under oxidative stress via the VEGF-R2/PI3K/Akt.

DC Field Value Language
dc.contributor.author권오웅-
dc.contributor.author변석호-
dc.contributor.author이성철-
dc.contributor.author이준행-
dc.contributor.author이형근-
dc.date.accessioned2015-04-23T16:22:48Z-
dc.date.available2015-04-23T16:22:48Z-
dc.date.issued2010-
dc.identifier.issn0146-0404-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/100476-
dc.description.abstractPURPOSE: Vascular endothelial cell growth factor (VEGF) is strongly induced by oxidative stress in retinal pigment epithelial (RPE) cells, and VEGF-A is a survival factor for various cell types. This study was conducted to determine whether the autocrine VEGF signaling pathway in RPE cells is involved in the mechanism of adaptive response to oxidative stress. METHODS: ARPE-19 cells were treated with hydrogen peroxide, and cell death was measured by flow cytometry with annexin V-fluorescein isothiocyanate. Survival analysis was performed with pretreatment of VEGF-A-neutralizing antibodies, VEGF receptor tyrosine kinase inhibitor (SU5416), or VEGF-A receptor-neutralizing antibodies (anti-VEGF-R1 and anti-VEGF-R2). The expression of VEGF-A, -R1, -R2, and soluble VEGF-R1 was determined by semiquantitative RT-PCR or Western blot analysis. Phosphorylation of VEGF-R2 was detected with immunoprecipitation and immunoblot analysis. RESULTS: Hydrogen peroxide-induced cell death was promoted by pretreatment with VEGF-A and anti-VEGF-R2-neutralizing antibodies, but not with anti-VEGF-R1-neutralizing antibody. Phosphorylation of VEGF-R2 in RPE cells was induced by hydrogen peroxide, and pretreatment with anti-VEGF-A-neutralizing antibody inhibited phosphorylation. Phosphorylation of Akt under oxidative stress was abrogated by pretreatment with neutralizing antibodies against either VEGF-A or SU5416. CONCLUSIONS: Autocrine VEGF-A enhanced RPE cell survival under oxidative stress; the autocrine VEGF-A/VEGF-R2/PI3K/Akt pathway is involved. Neutralization of VEGF-A signaling, as in eyes with age-related macular degeneration, may influence RPE cell survival.-
dc.description.statementOfResponsibilityopen-
dc.format.extent1190~1197-
dc.relation.isPartOfINVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHApoptosis-
dc.subject.MESHAutocrine Communication/physiology*-
dc.subject.MESHBlotting, Western-
dc.subject.MESHCell Culture Techniques-
dc.subject.MESHCell Survival-
dc.subject.MESHEnzyme-Linked Immunosorbent Assay-
dc.subject.MESHFlow Cytometry-
dc.subject.MESHFluorescent Antibody Technique, Indirect-
dc.subject.MESHHumans-
dc.subject.MESHHydrogen Peroxide/toxicity-
dc.subject.MESHOncogene Protein v-akt/metabolism-
dc.subject.MESHOxidative Stress*-
dc.subject.MESHPhosphatidylinositol 3-Kinases/metabolism-
dc.subject.MESHPhosphorylation-
dc.subject.MESHRetinal Pigment Epithelium/drug effects*-
dc.subject.MESHRetinal Pigment Epithelium/metabolism-
dc.subject.MESHReverse Transcriptase Polymerase Chain Reaction-
dc.subject.MESHVascular Endothelial Growth Factor A/metabolism*-
dc.subject.MESHVascular Endothelial Growth Factor Receptor-1/metabolism-
dc.subject.MESHVascular Endothelial Growth Factor Receptor-2/metabolism-
dc.titleVascular endothelial growth factor as an autocrine survival factor for retinal pigment epithelial cells under oxidative stress via the VEGF-R2/PI3K/Akt.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Ophthalmology (안과학)-
dc.contributor.googleauthorSuk Ho Byeon-
dc.contributor.googleauthorSung Chul Lee-
dc.contributor.googleauthorSoo Hyun Choi-
dc.contributor.googleauthorHyung-Keun Lee-
dc.contributor.googleauthorJoon H. Lee-
dc.contributor.googleauthorYoung Kwang Chu-
dc.contributor.googleauthorOh Woong Kwon-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00235-
dc.contributor.localIdA01849-
dc.contributor.localIdA02873-
dc.contributor.localIdA03180-
dc.contributor.localIdA03303-
dc.relation.journalcodeJ01187-
dc.identifier.eissn1552-5783-
dc.identifier.pmid19834034-
dc.contributor.alternativeNameKwon, Oh Woong-
dc.contributor.alternativeNameByeon, Suk Ho-
dc.contributor.alternativeNameLee, Sung Chul-
dc.contributor.alternativeNameLee, Joon Haeng-
dc.contributor.alternativeNameLee, Hyung Keun-
dc.contributor.affiliatedAuthorKwon, Oh Woong-
dc.contributor.affiliatedAuthorByeon, Suk Ho-
dc.contributor.affiliatedAuthorLee, Sung Chul-
dc.contributor.affiliatedAuthorLee, Joon Haeng-
dc.contributor.affiliatedAuthorLee, Hyung Keun-
dc.citation.volume51-
dc.citation.number2-
dc.citation.startPage1190-
dc.citation.endPage1197-
dc.identifier.bibliographicCitationINVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, Vol.51(2) : 1190-1197, 2010-
dc.identifier.rimsid36510-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Ophthalmology (안과학교실) > 1. Journal Papers

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