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Disrupted cell cycle arrest and reduced proliferation in corneal fibroblasts from GCD2 patients: a potential role for altered autophagy flux

DC FieldValueLanguage
dc.contributor.author김응권-
dc.contributor.author김태임-
dc.contributor.author맹용선-
dc.contributor.author최승일-
dc.date.accessioned2016-02-04T11:04:57Z-
dc.date.available2016-02-04T11:04:57Z-
dc.date.issued2015-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/139623-
dc.description.abstractThis study investigates the role of impaired proliferation, altered cell cycle arrest, and defective autophagy flux of corneal fibroblasts in granular corneal dystrophy type 2 (GCD2) pathogenesis. The proliferation rates of homozygous (HO) GCD2 corneal fibroblasts at 72 h, 96 h, and 120 h were significantly lower (1.102 ± 0.027, 1.397 ± 0.039, and 1.527 ± 0.056, respectively) than those observed for the wild-type (WT) controls (1.441±0.029, 1.758 ± 0.043, and 2.003 ± 0.046, respectively). Flow cytometry indicated a decreased G1 cell cycle progression and the accumulation of cells in the S and G2/M phases in GCD2 cells. These accumulations were associated with decreased levels of Cyclin A1, B1, and E1, and increased expression of p16 and p27. p21 and p53 expression was also significantly lower in GCD2 cells compared to the WT. Interestingly, treatment with the autophagy flux inhibitor, bafilomycin A1, resulted in similarly decreased Cyclin A1, B1, D1, and p53 expression in WT fibroblasts. Furthermore, similar findings, including a decrease in Cyclin A1, B1, and D1 and an increase in p16 and p27 expression were observed in autophagy-related 7 (Atg7; known to be essential for autophagy) gene knockout cells. These data provide new insight concerning the role of autophagy in cell cycle arrest and cellular proliferation, uncovering a number of novel therapeutic possibilities for GCD2 treatment.-
dc.description.statementOfResponsibilityopen-
dc.format.extent288~293-
dc.relation.isPartOfBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdolescent-
dc.subject.MESHAdult-
dc.subject.MESHAutophagy-
dc.subject.MESHCell Cycle Checkpoints*-
dc.subject.MESHCell Proliferation-
dc.subject.MESHChild-
dc.subject.MESHCornea/cytology*-
dc.subject.MESHCorneal Dystrophies, Hereditary/genetics-
dc.subject.MESHCorneal Dystrophies, Hereditary/metabolism-
dc.subject.MESHCorneal Dystrophies, Hereditary/pathology*-
dc.subject.MESHFemale-
dc.subject.MESHFibroblasts/drug effects*-
dc.subject.MESHFibroblasts/metabolism-
dc.subject.MESHFlow Cytometry-
dc.subject.MESHGene Expression Regulation*-
dc.subject.MESHHomozygote-
dc.subject.MESHHumans-
dc.subject.MESHMacrolides/chemistry-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHYoung Adult-
dc.titleDisrupted cell cycle arrest and reduced proliferation in corneal fibroblasts from GCD2 patients: a potential role for altered autophagy flux-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Ophthalmology (안과학)-
dc.contributor.googleauthorSeung-il Choi-
dc.contributor.googleauthorShorafidinkhuja Dadakhujaev-
dc.contributor.googleauthorYong-Sun Maeng-
dc.contributor.googleauthorSo-yeon Ahn-
dc.contributor.googleauthorTae-im Kim-
dc.contributor.googleauthorEung Kweon Kim-
dc.identifier.doi10.1016/j.bbrc.2014.11.073-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00831-
dc.contributor.localIdA01080-
dc.contributor.localIdA01346-
dc.contributor.localIdA04099-
dc.relation.journalcodeJ00281-
dc.identifier.eissn1090-2104-
dc.identifier.pmid25450621-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0006291X14021044-
dc.subject.keywordCell cycle arrest-
dc.subject.keywordCorneal fibroblasts-
dc.subject.keywordCyclin-
dc.subject.keywordDefective autophagy flux-
dc.subject.keywordGranular corneal dystrophy type 2-
dc.contributor.alternativeNameKim, Eung Kweon-
dc.contributor.alternativeNameKim, Tae Im-
dc.contributor.alternativeNameMaeng, Yong Sun-
dc.contributor.alternativeNameChoi, Seung Il-
dc.contributor.affiliatedAuthorKim, Eung Kweon-
dc.contributor.affiliatedAuthorKim, Tae Im-
dc.contributor.affiliatedAuthorMaeng, Yong Sun-
dc.contributor.affiliatedAuthorChoi, Seung Il-
dc.rights.accessRightsnot free-
dc.citation.volume456-
dc.citation.number1-
dc.citation.startPage288-
dc.citation.endPage293-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.456(1) : 288-293, 2015-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Ophthalmology (안과학교실) > 1. Journal Papers
5. Research Institutes (연구소) > Corneal Dystrophy Research Institute (각막이상증연구소) > 1. Journal Papers

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