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首页> 外文期刊>Journal of Cellular Physiology >Plasma membrane-dependent activation of gelatinase A in human vascular endothelial cells.
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Plasma membrane-dependent activation of gelatinase A in human vascular endothelial cells.

机译：等离子体membrane-dependent白明胶酶的激活一个在人类血管内皮细胞。

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The initiation of the angiogenic process requires a locally confined and time-limited proteolysis of the basement membrane (BM) components at the site of new vessel sprout. Gelatinase A, a member of the matrix metalloproteinase family, degrades BM type IV collagen and is involved in the BM breakdown by migrating tumor cells and endothelial cells (EC). Gelatinase A is synthesized as latent proenzyme and must be activated in order to express its proteolytic activity. A plasma membrane-dependent mechanism of activation has been described for several tumor and transformed cells lines. In the present study, we show that latent (72 kD) and mature (62-59 kD) forms of gelatinase A are present in EC membrane fraction from Triton X-114 extract while only latent form is found in the cytosolic fraction. The incubation of EC membrane fraction with exogenous latent gelatinase A resulted in a significant activation giving rise to 62-59 kD mature forms. 12-O-tetradecanoylphorbol-13-acetate (TPA), a strong potentiator of angiogenesis in vitro and in vivo, increases the amount of both latent and activated forms of gelatinase A in EC membrane fraction as well as the ability of this latter fraction to activate exogenous latent gelatinase A. We show that the mRNA transcript coding for the membrane-integrated MMP, the MT-MMP, previously described as a potential gelatinase A activator in invasive tumor cells is also expressed in vascular EC and is regulated through a TPA sensitive process. This enzyme may be responsible for membrane-dependent gelatinase A activation in normal vascular EC and may therefore be a determinant in the control of BM proteolysis during angiogenesis.
机译：血管生成的起始过程要求局部承压和有时限的蛋白水解作用基底膜(BM)组件的网站的新船发芽。基质金属蛋白酶家族的降解BM IV型胶原蛋白和大英博物馆肿瘤细胞迁移和崩溃内皮细胞(EC)。合成的潜在的酶原和必须激活为了表达蛋白水解活动。的激活被描述了肿瘤和转化细胞线。研究中,我们表明,潜在的(72 kD)和成熟(62 - 59 kD)白明胶酶的形式存在EC膜分数从特里同x - 114中提取虽然只在胞质中发现潜在的形式分数。外生潜在白明胶酶导致显著激活引起62 - 59 kD成熟的形式。12-O-tetradecanoylphorbol-13-acetate (TPA)强烈的体外血管生成和电位器体内,增加潜在的和激活形式的白明胶酶在EC膜分数以及后者的能力分数来激活外生潜在白明胶酶我们表明,该mRNA转录本编码membrane-integrated MMP MT-MMP,之前描述作为一个潜在的白明胶酶催化剂在侵入性肿瘤细胞也表示在血管EC和监管一个TPA敏感的过程。负责membrane-dependent白明胶酶激活在正常血管EC和可能因此,在BM的控制因素蛋白水解作用在血管生成。

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