Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-6-21
pubmed:abstractText
Clinical studies of drug-eluting stents delivering the mammalian target of rapamycin (mTOR) inhibitor, rapamycin (Sirolimus), have demonstrated a reduced efficacy for these devices in patients with diabetes, which suggests that the mTOR pathway may cease to be dominant in mediating the vascular response to injury under diabetic conditions. We hypothesized that changes in serum composition accompanying diabetes may reduce the role of mTOR in mediating the vascular response to injury. We measured the ability of a median dose of rapamycin (10 nM) to inhibit the proliferation of human coronary artery smooth muscle cells (huCASMCs) stimulated with serum obtained from donors with diabetes (n = 14) and without diabetes (n = 16). In an additional analysis, we compared the effects of rapamycin on huCASMCs stimulated with the serum of donors with metabolic syndrome (n = 15) versus those without (n = 7). There was no difference in the effect of rapamycin on huCASMC proliferation after stimulation with serum from either donors with diabetes or donors with metabolic syndrome compared with the respective controls. We conclude that the changes in the serum composition common to diabetes and metabolic syndrome are insufficient to diminish the role of mTOR in the progression of cardiovascular disease.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-10075613, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-10217658, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-12150925, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-12150926, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-14769686, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-15123524, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-15268862, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-16123336, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-16251229, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-16580520, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-17950788, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-18004109, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-7532117, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-8878442, http://linkedlifedata.com/resource/pubmed/commentcorrection/19129735-9430371
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1533-4023
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
86-9
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Sera from patients with diabetes do not alter the effect of mammalian target of rapamycin inhibition on smooth muscle cell proliferation.
pubmed:affiliation
Ochsner Clinic Foundation, New Orleans, LA 70121, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural