Nanopublications

Matches in Nanopublications for { ?s ?p ?o <http://www.tkuhn.ch/bel2nanopub/RAQA2IQrjwxnOb2yEhZZeBPBUHd9lH8XyG38gDEbvgrac#provenance>. }

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_5 label "Selventa" provenance.
large_corpus.bel title "BEL Framework Large Corpus Document" provenance.
_3 title "AHA Abstracts 1496" provenance.
_3 type "Other" provenance.
_3 identifier "AHA Abstracts 1496" provenance.
large_corpus.bel description "Approximately 61,000 statements." provenance.
large_corpus.bel version "20131211" provenance.
large_corpus.bel authoredBy _5 provenance.
assertion wasDerivedFrom large_corpus.bel provenance.
assertion wasDerivedFrom _4 provenance.
assertion hadPrimarySource _3 provenance.
_4 wasQuotedFrom _3 provenance.
_4 value "HMG-CoA reductase inhibitors have direct vascular effects that contribute to plaque stability. In the present study we demonstrate that the HMG-CoA reductase inhibitors atorvastatin and pravastatin augment the adhesion of human (HSMCs) and rat aortic smooth muscle cells (RASMCs) to collagen I via induction of alpha2beta1-integrin receptors. Atorvastatin (0.1 mcrM) increased the adhesion of HSMCs to collagen I up to 2-fold (p<0.01) and pravastatin (1.0 mcrM) up to 1.8-fold (p<0.01) after treatment for at least 24 hours. This increase in adhesion was concentration-dependent and was observed for treatment periods from 16 to 72 hours. Inhibition of isoprenoid synthesis with mevalonate and geranyl-geraniol prevented the statin-induced effect on human and rat smooth muscle cells. Flow cytometry revealed an increased expression of alpha2- and beta1-integrins after treatment with atorvastatin (0.1 mcrM) at 24 and 48 hours. Atorvastatin increased levels of b1-integrin mRNA after 12 and 24 hours treatment in HSMCs, which was inhibited by mevalonate. Furthermore, atorvastatin (0.1 mcrM) and pravastatin (1.0 mcrM) inhibited chemotaxis of HSMCs on collagen I, which was also reversed by mevalonate treatment. In contrast, inhibition of b1-integrins with a specific antibody nearly doubled (p<0.01) the rate of chemotaxis. These data indicate that the chemotactic activity in HSMCs is inhibited in part by upregulation of alpha2beta1-integrin receptors. The present study indicates that HMG-CoA reductase inhibitors increase cell-matrix interaction with collagen I via induction of a2b1-integrins and increased adhesion to collagen I" provenance.