Thrombospondin 1, Fibronectin, and Vitronectin are Differentially Dependent Upon RAS, ERK1/2, and p38 for Induction of Vascular Smooth Muscle Cell Chemotaxis

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  • Alliric I. Willis
    Yale University School of Medicine Section of Vascular Surgery, New Haven, CT, USA
  • Benjamin Sadowitz
    Division of Vascular Surgery and Endovascular Services, SUNY Upstate Medical University, Syracuse, NY, USA, Department of Veterans Affairs VA Healthcare Network Upstate New York at Syracuse, Syracuse, NY, USA
  • Shoichi Fuse
    Yale University School of Medicine Section of Vascular Surgery, New Haven, CT, USA
  • Kristopher G. Maier
    Division of Vascular Surgery and Endovascular Services, SUNY Upstate Medical University, Syracuse, NY, USA, Department of Veterans Affairs VA Healthcare Network Upstate New York at Syracuse, Syracuse, NY, USA
  • Tae S. Lee
    Yale University School of Medicine Section of Vascular Surgery, New Haven, CT, USA
  • Xiu-Jie Wang
    Yale University School of Medicine Section of Vascular Surgery, New Haven, CT, USA
  • George P. Tuszynski
    Temple University, Department of Neurovirology, Philadelphia, PA, USA
  • Bauer E. Sumpio
    Yale University School of Medicine Section of Vascular Surgery, New Haven, CT, USA, VA Connecticut Healthcare System, West Haven, CT, USA
  • Vivian Gahtan
    Yale University School of Medicine Section of Vascular Surgery, New Haven, CT, USA, Division of Vascular Surgery and Endovascular Services, SUNY Upstate Medical University, Syracuse, NY, USA, Department of Veterans Affairs VA Healthcare Network Upstate New York at Syracuse, Syracuse, NY, USA, VA Connecticut Healthcare System, West Haven, CT, USA,

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<jats:p> 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. </jats:p>

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