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首页> 外文期刊>Matrix biology: Journal of the International Society for Matrix Biology >Thrombospondins 1 and 2 function as inhibitors of angiogenesis.
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Thrombospondins 1 and 2 function as inhibitors of angiogenesis.

机译：血小板反应蛋白1和2充当血管生成的抑制剂。

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摘要

Thrombospondins (TSPs) 1 and 2 are matricellular proteins with the well-characterized ability to inhibit angiogenesis in vivo, and the migration and proliferation of cultured microvascular endothelial cells (ECs). Angiogenesis in developing tumors and in various models of wound healing is diminished or delayed by the presence of TSP1 or 2. Sequences within the type I repeats of TSP1 and 2 have been demonstrated to mediate the anti-migratory effects of TSPs on microvascular EC, although, paradoxically, sequences in the N- and C-terminal domains have pro-angiogenic effects. A scavenger receptor, CD36, recognizes the active sequences in the type I repeats, and is required for the anti-angiogenic effects of TSP1 in the corneal neovascularization assay. However, interactions of TSPs with growth factors, proteases, histidine-rich glycoprotein, and other cell-surface receptors on EC have the potential to modulate CD36-mediated effects. Binding of TSP1 to CD36 has been shown to activate apoptosis by inducing p38 and Jun N-terminal kinase, members of the mitogen-activated protein kinase superfamily, and subsequently the cell-surface expression of FasL. Ligation of Fas by FasL then induces a caspase cascade and apoptotic cell death. However, we have recently shown that inhibition of proliferation of microvascular EC by TSPs can occur in the absence of cell death. This finding raises the possibility that TSPs can activate separate cell death and anti-proliferative pathways.
机译：血小板反应蛋白（TSP）1和2是基质细胞蛋白，具有抑制体内血管生成以及培养的微血管内皮细胞（EC）迁移和增殖的特征。 TSP1或2的存在会减少或延迟正在发展的肿瘤和各种​​伤口愈合模型中的血管生成。尽管已证明TSP1和2的I型重复序列内的序列可介导TSP对微血管EC的抗迁移作用。矛盾的是，N-和C-末端结构域中的序列具有促血管生成作用。清道夫受体CD36识别I型重复序列中的活性序列，是TSP1在角膜新血管形成测定中的抗血管生成作用所必需的。但是，TSP与EC上的生长因子，蛋白酶，富含组氨酸的糖蛋白和其他细胞表面受体的相互作用具有调节CD36介导的作用的潜力。 TSP1与CD36的结合已显示出通过诱导p38和Jun N末端激酶（促分裂原激活的蛋白激酶超家族成员）并随后诱导FasL在细胞表面表达来激活细胞凋亡。 FasL连接Fas会诱导胱天蛋白酶级联反应和凋亡细胞死亡。但是，我们最近发现，在没有细胞死亡的情况下，TSP可以抑制微血管EC的增殖。这一发现增加了TSPs可以激活单独的细胞死亡和抗增殖途径的可能性。

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