PuSH - Publikationsserver des Helmholtz Zentrums München: ADAMTS-7 inhibits re-endothelialization of injured arteries and promotes vascular remodeling via cleavage of thrombospondin-1.

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Kessler, T.* ; Zhang, L.* ; Liu, Z.* ; Yin, X.* ; Huang, Y.* ; Wang, Y.* ; Fu, Y.* ; Mayr, M.* ; Ge, Q.* ; Xu, Q.* ; Zhu, Y.* ; Wang, X.* ; Schmidt, K.J.* ; de Wit, C.* ; Erdmann, J.* ; Schunkert, H.* ; Aherrahrou, Z* ; Kong, W.* ; German Mouse Clinic Consortium (Adamski, J. ; Adler, T. ; Aguilar-Pimentel, J.A. ; Amarie, O.V. ; Becker, L. ; Beckers, J. ; Brachthäuser, L. ; Busch, D.H. ; Calzada-Wack, J. ; Eickelberg, O. ; Fuchs, H. ; Gailus-Durner, V. ; Garrett, L. ; Graw, J. ; Hans, W. ; Hölter, S.M. ; Horsch, M. ; Hrabě de Angelis, M. ; Janik, D. ; Klein-Rodewald, T. ; Klingenspor, M. ; Klopstock, T. ; Lengger, C. ; Leuchtenberger, S. ; Maier, H. ; Moreth, K. ; Neff, F. ; Ollert, M. ; Prehn, C. ; Puk, O. ; Rathkolb, B. ; Rozman, J. ; Steinkamp, R. ; Stoeger, C. ; Stöger, T. ; Vernaleken, A. ; Yildirim, A.Ö. ; Wurst, W. ; Zimprich, A.)

ADAMTS-7 inhibits re-endothelialization of injured arteries and promotes vascular remodeling via cleavage of thrombospondin-1.

Circulation 131, 1191-1201 (2015)

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BACKGROUND: -ADAMTS-7, a member of the disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family, is recently identified to be genome-wide significantly associated with coronary artery disease (CAD). However, the mechanisms that link ADAMTS-7 and CAD risk remain elusive. We have previously demonstrated that ADAMTS-7 promotes vascular smooth muscle cell migration and post-injury neointima formation via degradation of a matrix protein cartilage oligomeric matrix protein (COMP). Because delayed endothelium repair renders neointima and atherosclerosis plaque formation after vessel injury, we examined whether ADAMTS-7 also inhibits re-endothelialization. METHODS AND RESULTS: -Wire-injury of the carotid artery and Evans blue staining were performed in Adamts7(-/-) and wildtype mice. Adamts-7 deficiency greatly promoted re-endothelialization at 3, 5, and 7 days after injury. Consequently, Adamts-7 deficiency substantially ameliorated neointima formation in mice at days 14 and 28 after injury compared with the wildtype. In vitro studies further indicated that ADAMTS-7 inhibited both endothelial cell proliferation and migration. Surprisingly, COMP deficiency did not affect endothelial cell proliferation/migration and re-endothelialization in mice. In a further examination of other potential vascular substrates of ADAMTS-7, a label-free LC MS/MS secretome analysis revealed thrombospondin-1 (TSP-1) as a potential ADAMTS-7 target. The subsequent studies showed that ADAMTS-7 was directly associated with TSP-1 by its C-terminus and degraded TSP-1 in vivo and in vitro. The inhibitory effect of ADAMTS-7 on post-injury endothelium recovery was circumvented in Tsp1(-/-) mice. CONCLUSIONS: -Our study revealed a novel mechanism by which ADAMTS-7 affects neointima formation. Thus, ADAMTS-7 is a promising treatment target for post-injury vascular intima hyperplasia.

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