Linked Life Data

17597576

Source:http://linkedlifedata.com/resource/pubmed/id/17597576

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-8-27
pubmed:abstractText
High glucose inhibits endothelial cell proliferation. Thus, we studied cyclin-dependent kinase inhibitor p15(INK4b) in high glucose-induced effects in human umbilical endothelial cells at 24h. High glucose decreased cell proliferation while arresting cells in G(0)/G(1) phase of the cell cycle. High glucose increased phospho-extracellular signal regulated kinase (ERK)1/2, p15(INK4b) protein and mRNA expression. High glucose-inhibited cell proliferation was attenuated by antisense p15(INK4b) oligonucleotide. Moreover, PD98059 attenuated high glucose-induced p15(INK4b) protein expression. High glucose increased transforming growth factor-beta (TGF-beta) gene transcriptional activity and mRNA expression. However, neither SB431542 (type I TGF-beta receptor blocker) nor TGF-beta1 antibody affected high glucose-induced p15(INK4b) protein expression. Additionally, N-acetylcysteine (an antioxidant) attenuated high glucose-induced growth arrest and p15(INK4b) protein expression. Thus, high glucose-induced growth arrest is dependent on p15(INK4b) and oxidative stress in endothelial cells. Moreover, high glucose-induced p15(INK4b) protein expression is dependent on ERK1/2 and oxidative stress.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0003-9861
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
465
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
164-71
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
High glucose decreases endothelial cell proliferation via the extracellular signal regulated kinase/p15(INK4b) pathway.
pubmed:affiliation
Graduate Institute of Medicine, Faculty of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't