Linked Life Data

20731356

Source:http://linkedlifedata.com/resource/pubmed/id/20731356

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2010-9-15
pubmed:abstractText
Abnormal proliferation of vascular smooth muscle cells (VSMCs) plays a central role in the pathogenesis of atherosclerosis. ?-Sitosterol, an important phytosterol found in plant food, is known to exert antiatherosclerosis activity. However, the molecular mechanisms underlying ?-sitosterol-induced antiproliferation of VSMCs were still not clear. This study demonstrated that ?-sitosterol (1-20 ?M) concentration-dependently inhibited proliferation of rat aortic smooth muscle cells (RASMCs) without cytotoxic effect. Flow cytometric analysis revealed that ?-sitosterol arrested cell cycle progression through down-regulation of cyclin E and cyclin-dependent kinase (CDK)2 and up-regulation of p21cip1. In the ?-sitosterol-treated RASMCs, the formation of the CDK2-p21cip1 complex was increased and the assayable CDK2 activity was decreased. Knockdown of the expression of p21cip1 gene prevented ?-sitosterol-induced cell cycle arrest in RASMCs. In conclusion, ?-sitosterol inhibited VSMC proliferation by increasing the levels of p21cip1 protein, which in turn inhibited the CDK2 activity, and finally interrupted the progress of the cell cycle.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1520-5118
pubmed:author
pubmed:issnType
Electronic
pubmed:day
22
pubmed:volume
58
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
10064-9
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
?-Sitosterol inhibits cell cycle progression of rat aortic smooth muscle cells through increases of p21cip1 protein.
pubmed:affiliation
Taipei Medical University-Wang-Fang Hospital, Taipei, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't