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http://purl.uniprot.org/citations/21193465http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21193465http://www.w3.org/2000/01/rdf-schema#comment"

Background

Thrombospondin 1 (TSP-1), fibronectin (Fn), and vitronectin (Vn) promote vascular smooth muscle cell (VSMC) chemotaxis through a variety of second messenger systems, including Ras, ERK1/2, and p38.

Hypothesis

Ras, ERK1/2, and p38 differentially affect TSP-1-, Fn-, and Vn-induced VSMC chemotaxis.

Methods

Bovine VSMCs were transfected with Ras N17 or treated with the following inhibitors: a farnesyl protein transferase (FPT) inhibitor, PD098059 (ERK1/2 inhibitor), or SB202190 (p38 inhibitor). Thrombospondin 1, Fn, and Vn were used as chemoattractants. Results were analyzed by analysis of variance (ANOVA) with post hoc testing (P < .05).

Results

Ras N17 transfection or FPT inhibitor treatment inhibited TSP-1-, Fn-, and Vn-induced chemotaxis. PD098059 or SB202190 resulted in more inhibition of VSMC migration to TSP-1 than to Fn or Vn.

Conclusions

Ras appears equally relevant in the signal transduction pathways of TSP-1-, Fn-, and Vn-induced VSMC chemotaxis. Thrombospondin 1-induced migration is more dependent upon ERK1/2 and p38 than Fn- or Vn-included migration."xsd:string
http://purl.uniprot.org/citations/21193465http://purl.org/dc/terms/identifier"doi:10.1177/1538574410387677"xsd:string
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/author"Wang X.J."xsd:string
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/author"Lee T.S."xsd:string
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/author"Fuse S."xsd:string
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/author"Tuszynski G.P."xsd:string
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/author"Sumpio B.E."xsd:string
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/author"Maier K.G."xsd:string
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/author"Gahtan V."xsd:string
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/author"Willis A.I."xsd:string
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/author"Sadowitz B."xsd:string
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/name"Vasc Endovascular Surg"xsd:string
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/pages"55-62"xsd:string
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/title"Thrombospondin 1, fibronectin, and vitronectin are differentially dependent upon RAS, ERK1/2, and p38 for induction of vascular smooth muscle cell chemotaxis."xsd:string
http://purl.uniprot.org/citations/21193465http://purl.uniprot.org/core/volume"45"xsd:string
http://purl.uniprot.org/citations/21193465http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21193465
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