Inhibition of phosphatidylinositol 3-kinase and protein kinase C attenuates extracellular matrix protein-induced vascular smooth muscle cell chemotaxis

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Presentation transcript:

Inhibition of phosphatidylinositol 3-kinase and protein kinase C attenuates extracellular matrix protein-induced vascular smooth muscle cell chemotaxis Alliric I. Willis, MD, Shoichi Fuse, MD, Xiu Jie Wang, MD, Emery Chen, BA, George P. Tuszynski, PhD, Bauer E. Sumpio, MD, PhD, Vivian Gahtan, MD Journal of Vascular Surgery Volume 31, Issue 6, Pages 1160-1167 (June 2000) DOI: 10.1067/mva.2000.106489 Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 1 Chemotaxis concentration curve for LY 294002. Preincubation of vascular smooth muscle cells with the phosphatidylinositol 3-kinase inhibitor LY 294002 (10, 50, and 100 μmol/L) demonstrated significant inhibition of thrombospondin-1 (TSP-1 )-, fibronectin (Fn )-, and vitronectin (Vn )-induced chemotaxis at 50 and 100 μmol/L. *P <.05 and **P <.005, compared with their respective uninhibited vascular smooth muscle cell chemotaxis toward TSP-1, Fn, or Vn. A representative experiment is shown. Journal of Vascular Surgery 2000 31, 1160-1167DOI: (10.1067/mva.2000.106489) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 2 Attenuation of vascular smooth muscle cell chemotaxis by phosphatidylinositol 3-kinase inhibition. Preincubation of vascular smooth muscle cells with the phosphatidylinositol 3-kinase inhibitor LY 294002 (100 μmol/L) significantly attenuated vascular smooth muscle cell chemotaxis toward thrombospondin-1 (TSP-1 ), fibronectin (Fn ), and vitronectin (Vn ), to a level not significantly different from vascular smooth muscle cells exposed to serum-free media (SFM ), P <.05. The chemoattractants TSP-1, Fn, and Vn (20 μg/mL) induced a significant increase in chemotaxis of uninhibited vascular smooth muscle cells, in comparison with SFM (P <.05). LY 294002 had no significant effect on the migration of vascular smooth muscle cells exposed to SFM. A representative experiment is shown. Experiments were performed in triplicate and repeated at least three times. *P <.05, compared with their respective uninhibited vascular smooth muscle cell chemotaxis toward TSP-1, Fn, or Vn. Journal of Vascular Surgery 2000 31, 1160-1167DOI: (10.1067/mva.2000.106489) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 3 Chemotaxis concentration curve for GF 109203X. Preincubation of vascular smooth muscle cells with the protein kinase C inhibitor GF 109203X (100 nmol/L, 1 μmol/L, and 5 μmol/L) demonstrated significant inhibition of thrombospondin-1 (TSP-1 )–induced chemotaxis at 1 and 5 μmol/L. *P <.05, compared with their respective uninhibited vascular smooth muscle cells chemotaxis toward TSP-1, Fn, or Vn. A representative experiment is shown. Journal of Vascular Surgery 2000 31, 1160-1167DOI: (10.1067/mva.2000.106489) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 4 Attenuation of vascular smooth muscle cell chemotaxis by protein kinase C inhibition. Preincubation of vascular smooth muscle cells with the protein kinase C inhibitor GF 109203X (1 μmol/L) significantly attenuated vascular smooth muscle cell chemotaxis toward thrombospondin-1 (TSP-1 ; P <.05). The chemoattractants TSP-1, fibronectin (Fn ), and vitronectin (Vn ; 20 μg/mL) induced a significant increase in chemotaxis of uninhibited vascular smooth muscle cells in comparison with serum-free media (SFM ; P <.05). GF 109203X had no significant effect on migration of vascular smooth muscle cells exposed to SFM. A representative experiment is shown. Experiments were performed in triplicate and repeated at least three times. *P <.05, compared with their respective uninhibited vascular smooth muscle cell chemotaxis toward TSP-1, Fn, or Vn. Journal of Vascular Surgery 2000 31, 1160-1167DOI: (10.1067/mva.2000.106489) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions

Fig. 5 A schematic representation of the potential involvement of phosphatidylinositol 3-kinase (PI3K ) and protein kinase C (PKC ) in thrombospondin-1 (TSP-1 )-, fibronectin (Fn )-, and vitronectin (Vn )-induced vascular smooth muscle cell (VSMC ) chemotaxis. PI3K may serve as an important signal transducer in chemotaxis triggered by the binding of TSP-1, Fn, or Vn. PI3K may relay its signaling via its interaction with G proteins, Ras, or mitogen-activated protein kinase (MAPK ). PKC is likely involved in signal transduction in TSP-1-induced VSMC chemotaxis, but not that of Fn or Vn. Journal of Vascular Surgery 2000 31, 1160-1167DOI: (10.1067/mva.2000.106489) Copyright © 2000 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter Terms and Conditions