Thrombospondin 2 Modulates Collagen Fibrillogenesis and Angiogenesis

摘要: Thrombospondin 2 (TSP2)-null mice, generated by targeted disruption of the Thbs2 gene, display a complex phenotype that is characterized, in part, variety connective tissue abnormalities and increased vascular density skin subcutaneous tissues. In this paper we summarize evidence TSP2 functions as matricellular protein to influence cell function modulating cell–matrix interactions, rather than acting an integral component matrix. Thus, structurally abnormal collagen fibrils detected appear be consequence defective adhesion demonstrated dermal fibroblasts culture that, turn, result from matrix metalloproteinase (MMP2, gelatinase A) production these cells. Corroborating for such mode action comes transmission electron microscopic images developing flexor muscle tendons show distinct fibroblast–collagen fibril interactions TSP2-null tissue. The seen mice can reproduced number models injury, including implantation polyvinyl alcohol sponges silicone rubber discs, excisional wounds. Experiments are proposed distinguish between primarily endothelial versus extracellular origin angiogenesis mice.