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Mitomycin C induces apoptosis in cultured corneal fibroblasts derived from type II granular corneal dystrophy corneas.

DC FieldValueLanguage
dc.contributor.author김응권-
dc.contributor.author김태임-
dc.contributor.author이형근-
dc.contributor.author조영재-
dc.contributor.author최승일-
dc.date.accessioned2015-05-19T16:31:02Z-
dc.date.available2015-05-19T16:31:02Z-
dc.date.issued2008-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/106452-
dc.description.abstractPURPOSE: The present study investigated the effect of mitomycin C (MMC) on cell viability, apoptosis, and transforming growth factor beta-induced protein (TGFBIp) expression in cultured normal corneal fibroblasts and heterozygote or homozygote granular corneal dystrophy type II (GCD II) corneal fibroblasts. METHODS: Keratocytes were obtained from normal cornea or from heterozygote or homozygote GCD II patients after lamellar or penetrating keratoplasty. To measure cell viability, corneal fibroblasts were incubated with 0.02% MMC for 3 h, 6 h, and 24 h or with 0%, 0.01%, 0.02%, and 0.04% MMC for 24 h and then tested using lactate dehydrogenase (LDH) and 3-[4,5-demethylthiazol-2,5-diphenyl-2H-tetrazolium bromide] (MTT) assays. To measure apoptosis, cells were analyzed by FACS analysis and annexin V staining. Bcl-xL, Bax, and TGFBI mRNA expression was measured using reverse transcription polymerase chain reaction (RT-PCR) assays. Cellular and media levels of TGFBIp protein were measured by immunoblotting. RESULTS: MTT and LDH assays showed that MMC reduced cell viability in all three cell types in a dose-dependent and time-dependent manner (p<0.05). FACS analysis and annexin V staining showed that MMC caused apoptosis with GCD II homozygote cells being most affected. RT-PCR analysis showed that MMC decreased Bcl-xL mRNA expression and increased Bax mRNA expression in all cell types. RT-PCR and immunoblotting analysis showed that MMC reduced TGFBI mRNA levels and cellular and media TGFBIp protein levels in all cell types. CONCLUSIONS: MMC induced apoptosis, and the effects of MMC were greatest in GCD II homozygote cells. MMC also reduced the production of TGFBIp in all three types of corneal fibroblasts. These findings may explain the additional therapeutic effect of MMC in GCD II patients.-
dc.description.statementOfResponsibilityopen-
dc.format.extent1222~1228-
dc.relation.isPartOfMOLECULAR VISION-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHApoptosis/drug effects*-
dc.subject.MESHCell Survival/drug effects-
dc.subject.MESHCells, Cultured-
dc.subject.MESHCornea/pathology*-
dc.subject.MESHCorneal Dystrophies, Hereditary/pathology*-
dc.subject.MESHDose-Response Relationship, Drug-
dc.subject.MESHExtracellular Matrix Proteins/genetics-
dc.subject.MESHExtracellular Matrix Proteins/metabolism-
dc.subject.MESHFibroblasts/drug effects*-
dc.subject.MESHFibroblasts/pathology*-
dc.subject.MESHGene Expression Regulation/drug effects-
dc.subject.MESHHumans-
dc.subject.MESHMitomycin/pharmacology*-
dc.subject.MESHRNA, Messenger/genetics-
dc.subject.MESHRNA, Messenger/metabolism-
dc.subject.MESHTime Factors-
dc.subject.MESHTransforming Growth Factor beta/genetics-
dc.subject.MESHTransforming Growth Factor beta/metabolism-
dc.subject.MESHbcl-2-Associated X Protein/genetics-
dc.subject.MESHbcl-2-Associated X Protein/metabolism-
dc.titleMitomycin C induces apoptosis in cultured corneal fibroblasts derived from type II granular corneal dystrophy corneas.-
dc.typeArticle-
dc.contributor.collegeResearcher Institutes (부설 연구소)-
dc.contributor.departmentCorneal Dystrophy Research Institute (각막이상증연구소)-
dc.contributor.googleauthorTae-im Kim-
dc.contributor.googleauthorSeung-il Choi-
dc.contributor.googleauthorHyung Keun Lee-
dc.contributor.googleauthorYoung Jae Cho-
dc.contributor.googleauthorEung Kweon Kim-
dc.identifier.doi18615204-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00831-
dc.contributor.localIdA01080-
dc.contributor.localIdA03303-
dc.contributor.localIdA03858-
dc.contributor.localIdA04099-
dc.relation.journalcodeJ02272-
dc.identifier.eissn1090-0535-
dc.identifier.pmid18615204-
dc.subject.keywordApoptosis/drug effects*-
dc.subject.keywordCell Survival/drug effects-
dc.subject.keywordCells, Cultured-
dc.subject.keywordCornea/pathology*-
dc.subject.keywordCorneal Dystrophies, Hereditary/pathology*-
dc.subject.keywordDose-Response Relationship, Drug-
dc.subject.keywordExtracellular Matrix Proteins/genetics-
dc.subject.keywordExtracellular Matrix Proteins/metabolism-
dc.subject.keywordFibroblasts/drug effects*-
dc.subject.keywordFibroblasts/pathology*-
dc.subject.keywordGene Expression Regulation/drug effects-
dc.subject.keywordHumans-
dc.subject.keywordMitomycin/pharmacology*-
dc.subject.keywordRNA, Messenger/genetics-
dc.subject.keywordRNA, Messenger/metabolism-
dc.subject.keywordTime Factors-
dc.subject.keywordTransforming Growth Factor beta/genetics-
dc.subject.keywordTransforming Growth Factor beta/metabolism-
dc.subject.keywordbcl-2-Associated X Protein/genetics-
dc.subject.keywordbcl-2-Associated X Protein/metabolism-
dc.contributor.alternativeNameKim, Eung Kweon-
dc.contributor.alternativeNameKim, Tae Im-
dc.contributor.alternativeNameLee, Hyung Keun-
dc.contributor.alternativeNameCho, Young Jae-
dc.contributor.alternativeNameChoi, Seung Il-
dc.contributor.affiliatedAuthorKim, Eung Kweon-
dc.contributor.affiliatedAuthorKim, Tae Im-
dc.contributor.affiliatedAuthorLee, Hyung Keun-
dc.contributor.affiliatedAuthorCho, Young Jae-
dc.contributor.affiliatedAuthorChoi, Seung Il-
dc.rights.accessRightsfree-
dc.citation.volume14-
dc.citation.startPage1222-
dc.citation.endPage1228-
dc.identifier.bibliographicCitationMOLECULAR VISION, Vol.14 : 1222-1228, 2008-
Appears in Collections:
5. Research Institutes (연구소) > Corneal Dystrophy Research Institute (각막이상증연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Ophthalmology (안과학교실) > 1. Journal Papers

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