https://scholars.lib.ntu.edu.tw/handle/123456789/567281
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | Tsui L. | en_US |
dc.contributor.author | Fong T.-H. | en_US |
dc.contributor.author | I-JONG WANG | en_US |
dc.date.accessioned | 2021-07-01T01:06:47Z | - |
dc.date.available | 2021-07-01T01:06:47Z | - |
dc.date.issued | 2012 | - |
dc.identifier.issn | 1090-0535 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84863322445&partnerID=40&md5=705b18cb53e2066c668afe9eaa175d62 | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/567281 | - |
dc.description.abstract | Purpose: The survival of retinal ganglion cells (RGCs) is a hallmark of many optic neurodegenerative diseases such as glaucoma. YC-1, a potential anticancer drug, is known to be able to decrease the stability and protein expression of hypoxiainducible factor (HIF)-1α that is triggered by hypoxia and related to RGC survival. We hypothesized that YC-1 may alter RGC cell viability through the down-regulation of HIF-1α. Methods: Cell viability of the RGC-5 cell line was measured with a 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Flow cytometry, a LIVE/DEAD viability assay, and high-content screening (HCS) with MKI67 (K i-67) monoclonal antibodies were used to detect cell death and cellular proliferation. Results: We found that cells treated with 20 μM YC-1 for 24 h decreased the HIF-1α level in an RGC-5 cell line using immunoblotting and reduced the live cell number in an MTT assay. Results of flow cytometry and HCS demonstrated that reducing the cell proliferation of RGC-5 cells, not cell death, led to the decreased level in the MTT assay. Conclusions: Our findings demonstrate that YC-1-induced down-regulation of HIF-1α might reduce RGC cell proliferation and viability under normoxia, which implies a role of YC-1 in the neuroprotective effect for further clinical applications. ? 2012 Molecular Vision. | - |
dc.relation.ispartof | Molecular Vision | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | hypoxia inducible factor 1alpha; lificiguat; apoptosis; article; cell count; cell death; cell level; cell proliferation; cell viability; controlled study; down regulation; drug mechanism; priority journal; retina ganglion cell; Antibodies; Antineoplastic Agents; Apoptosis; Cell Line; Cell Proliferation; Cell Survival; Dose-Response Relationship, Drug; Down-Regulation; Humans; Hypoxia-Inducible Factor 1, alpha Subunit; Indazoles; Ki-67 Antigen; Retinal Ganglion Cells; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Signal Transduction | - |
dc.title | YC-1 targeting of hypoxia-inducible factor-1α reduces RGC-5 cell viability and inhibits cell proliferation | en_US |
dc.type | journal article | en |
dc.identifier.pmid | 22736948 | - |
dc.identifier.scopus | 2-s2.0-84863322445 | - |
dc.relation.pages | 1594-1603 | - |
dc.relation.journalvolume | 18 | - |
item.fulltext | no fulltext | - |
item.openairetype | journal article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | Ophthalmology | - |
crisitem.author.dept | Ophthalmology-NTUH | - |
crisitem.author.dept | Division of Cornea | - |
crisitem.author.orcid | 0000-0002-3045-0614 | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | Ophthalmology-NTUH | - |
顯示於: | 醫學系 |
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