Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-12-6
pubmed:abstractText
Aspirin is a common preventative therapy in patients at risk for cardiovascular diseases, yet little is known about how aspirin protects the vasculature in hypercholesterolemia. The present study determines whether aspirin, nitric oxide-releasing aspirin (NCX-4016), a selective cyclooxygenase (COX)-1 inhibitor (SC560), or genetic deficiency of COX-1 prevents the inflammatory and prothrombogenic phenotype assumed by hypercholesterolemic (HC) venules. Aspirin or NCX-4016 (60 mg/kg) was administered orally for the last week of a 2-wk HC diet. COX-1-deficient (COX-1(-/-)) and wild-type (WT) mice were transplanted with WT (WT/COX-1(-/-)) or COX-1(-/-) (COX-1(-/-)/WT) bone marrow, respectively. HC-induced adhesion of platelets and leukocytes in murine intestinal venules, observed with intravital fluorescence microscopy, was greatly attenuated in aspirin-treated mice. Adhesion of aspirin-treated platelets in HC venules was comparable to untreated platelets, whereas adhesion of SC560-treated platelets was significantly attenuated. HC-induced leukocyte and platelet adhesion in COX-1(-/-)/WT chimeras was comparable to that in SC560-treated mice, whereas the largest reductions in blood cell adhesion were in WT/COX-1(-/-) chimeras. NCX-4016 treatment of platelet recipients or donors attenuated leukocyte and platelet adhesion independent of platelet COX-1 inhibition. Platelet- and endothelial cell-associated COX-1 promote microvascular inflammation and thrombogenesis during hypercholesterolemia, yet nitric oxide-releasing aspirin directly inhibits platelets independent of COX-1.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
293
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H3636-42
pubmed:meshHeading
pubmed-meshheading:17933963-Animals, pubmed-meshheading:17933963-Aspirin, pubmed-meshheading:17933963-Blood Platelets, pubmed-meshheading:17933963-Bone Marrow Transplantation, pubmed-meshheading:17933963-Cardiovascular Diseases, pubmed-meshheading:17933963-Cell Adhesion, pubmed-meshheading:17933963-Chimera, pubmed-meshheading:17933963-Cholesterol, Dietary, pubmed-meshheading:17933963-Cyclooxygenase 1, pubmed-meshheading:17933963-Cyclooxygenase Inhibitors, pubmed-meshheading:17933963-Disease Models, Animal, pubmed-meshheading:17933963-Endothelial Cells, pubmed-meshheading:17933963-Endothelium, Vascular, pubmed-meshheading:17933963-Hypercholesterolemia, pubmed-meshheading:17933963-Leukocytes, pubmed-meshheading:17933963-Male, pubmed-meshheading:17933963-Membrane Proteins, pubmed-meshheading:17933963-Mice, pubmed-meshheading:17933963-Mice, Inbred C57BL, pubmed-meshheading:17933963-Mice, Knockout, pubmed-meshheading:17933963-Microscopy, Fluorescence, pubmed-meshheading:17933963-Microscopy, Video, pubmed-meshheading:17933963-Nitric Oxide Donors, pubmed-meshheading:17933963-Platelet Adhesiveness, pubmed-meshheading:17933963-Pyrazoles, pubmed-meshheading:17933963-Venules
pubmed:year
2007
pubmed:articleTitle
Roles of platelet and endothelial cell COX-1 in hypercholesterolemia-induced microvascular dysfunction.
pubmed:affiliation
Department of Molecular and Cellular Physiology, Health Sciences Center, Louisiana State University, 1501 Kings Highway, Shreveport, LA 71130-3932, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural