Linked Life Data

16025229

Source:http://linkedlifedata.com/resource/pubmed/id/16025229

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-7-18
pubmed:abstractText
An important issue in atherosclerosis is the timing of intimal microvascular formation and its relation to the initiation of plaque formation. Monocytes and endothelial cells (ECs) are important cell components in these steps. Statins not only reduce atherogenic low density lipoprotein cholesterol, they also increase high density lipoprotein-cholesterol (HDL). Although a higher concentration of statin has an anti-proliferative effect, HDL is potentially mitogenic. Therefore, we examined the opposing effects of statin, Apo-AI, HDL and HDL fractions on cell proliferation and apoptosis in monocytes and on angiogenesis in ECs. A high concentration of simvastatin inhibited monocyte proliferation as evaluated by counting cell numbers using a hematocytometer. This inhibition was mainly blocked by the HDL3 subfraction. The same concentration of simvastatin induced apoptosis as assessed by the fluorescence-labeled annexin-V method through caspase-3 activation in monocytes. HDL inhibited simvastatin-induced apoptosis. In addition, HDL blocked simvastatin-inhibited angiogenesis in an in vitro model of EC tube formation. In conclusion, the compensatory balance between the effects of statin and HDL may play an important role in the formation of atherosclerotic lesions by affecting proliferation and apoptosis in monocytes and angiogenesis in ECs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0920-3206
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
113-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Counteracting effects of high density lipoprotein-cholesterol subfractions on statin-induced growth arrest.
pubmed:affiliation
Department of Cardiology, Fukuoka University School of Medicine, Fukuoka, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't