Susan M. Nesselroth, MDa, Alliric I

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The C-terminal domain of thrombospondin-1 induces vascular smooth muscle cell chemotaxis Susan M. Nesselroth, MDa, Alliric I. Willis, MDa, Shoichi Fuse, MDa, Eric T. Olson, BAa, Jack Lawler, PhDb, Bauer E. Sumpio, MD, PhDa, Vivian Gahtan, MDa Journal of Vascular Surgery Volume 33, Issue 3, Pages 595-600 (March 2001) DOI: 10.1067/mva.2001.112318 Copyright © 2001 Society for Vascular Surgery and The American Association for Vascular Surgery Terms and Conditions

Fig. 1 TSP-1 is composed of three identical chains linked together by disulfide bonds at PCH domain. Each chain can be divided into six domains of repeating homologous amino acid sequences: N-terminal (NH2), procollagen homology (PCH ), type 1 repeat (T1 ), type 2 repeat (T2 ), type 3 repeat/RGD (T3 ), and C-terminal (COOH ). Journal of Vascular Surgery 2001 33, 595-600DOI: (10.1067/mva.2001.112318) Copyright © 2001 Society for Vascular Surgery and The American Association for Vascular Surgery Terms and Conditions

Fig. 2 Fusion protein-induced VSMC chemotaxis. Fusion proteins to six domains of TSP-1 were tested for their ability to induce VSMC chemotaxis. Figure shows representative experiment of fusion protein-induced VSMC chemotaxis. Fusion proteins (10 and 20 μg/mL) are listed across x-axis. The y-axis shows number of cells migrating to undersurface of the membrane for each of the fusion proteins; SFM was used as negative control. Three experiments were performed for each of the fusion proteins (n = 3). The C-terminal domain (COOH ) and N-terminal domain (NH2) induced VSMC chemotaxis to a significant degree at 10 and 20 μg/mL (COOH: P = <.0001 at both concentrations; NH2: P =.007 for 10 μg/mL and P =.001 for 20 μg/mL). The type 3 repeat domain (T3 ) also induced chemotaxis but to a much lesser degree than COOH or NH2, and only at 20 μg/mL did degree of VSMC chemotaxis reach statistical significance (P =.028). Fusion proteins to the remaining three domains had no effect on VSMC chemotaxis. PCH, Procollagen homology; SFM, serum-free medium; T1, type 1 repeat; T2, type 2 repeat; TSP-1, thrombospondin-1. Journal of Vascular Surgery 2001 33, 595-600DOI: (10.1067/mva.2001.112318) Copyright © 2001 Society for Vascular Surgery and The American Association for Vascular Surgery Terms and Conditions

Fig. 3 Inhibition of TSP-1-induced chemotaxis by anti–TSP-1 domain antibodies. mAbs directed against domains of TSP-1 were tested for their ability to inhibit TSP-1–induced VSMC chemotaxis. Anti-COOH mAb (C6.7) and anti-IAP portion of COOH mAb (D4.6) significantly inhibited TSP-1–induced VSMC chemotaxis to 15% and 8% of TSP-1 alone, respectively. In other words, these mAbs inhibited TSP-1–induced VSMC chemotaxis by 85% and 92% (P <.05). The amount of inhibition by these two mAbs is similar to inhibition obtained by polyclonal anti–TSP-1 antibody, which reduced TSP-1–induced chemotaxis to 13% of TSP-1 alone (ie, an 87% inhibition of TSP-1–induced VSMC chemotaxis). Remaining mAbs resulted in no significant inhibition of TSP-1–induced VSMC chemotaxis. Anti-T1 IgM mAb, however, was noted to stimulate VSMC chemotaxis to greater degree than control, 118% of TSP-1 alone. COOH, C-terminal; NH2, N-terminal; T1, type 1 repeat; T2, type 2 repeat; TSP-1, thrombospondin-1. Journal of Vascular Surgery 2001 33, 595-600DOI: (10.1067/mva.2001.112318) Copyright © 2001 Society for Vascular Surgery and The American Association for Vascular Surgery Terms and Conditions