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首页> 外文期刊>Endothelium: Journal of endothelial cell research >Regulation of extracellular matrix remodeling and MMP-2 activation in cultured rat adrenal medullary endothelial cells.
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Regulation of extracellular matrix remodeling and MMP-2 activation in cultured rat adrenal medullary endothelial cells.

机译：培养的大鼠肾上腺髓质内皮细胞中细胞外基质重塑和MMP-2激活的调控。

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We previously reported that short-term exposure of cultured rat adrenal medullary endothelial cells (RAMEC) to thrombin enhances the subendothelial deposition of extracellular matrix (ECM) proteins fibronectin, laminin, and collagen types I (C-I) and IV (C-IV) (Papadimitriou et al. 1997). In this work, we extended our previous studies on factors that effect ECM protein deposition to include agents that activate or inhibit some of the most common intracellular signals such as cAMP, protein kinase C (PKC), and calcium. Furthermore, we investigated the possible link between the observed alterations in ECM protein deposition and the secretion of matrix metalloproteinase-2 (MMP-2). Forskolin (adenylyl cyclase activator) caused a dose-dependent increase in the deposition of all four ECM proteins studied. Isoproterenol beta-adrenergic receptor agonist) and the membrane permeant cAMP analogue dibutyryl-cAMP significantly increased the deposited amounts of ECM proteins at low concentrations, and this increase was reversed at higher concentrations of both agents. All these agents had the opposite effect on MMP-2 secretion, increasing it at doses where they decreased ECM protein deposition and vice versa. However, elevation of cAMP by the phosphodiesterase inhibitor IBMX had no effect either on the deposited amounts of any of the ECM proteins studied or on MMP-2 secretion. Activation of PKC by phorbol ester (PMA) resulted in a decrease in ECM protein deposition and an increase in MMP-2 secretion. Finally, chelation of intercellular calcium with BAPTA-AM resulted in an increased ECM deposition and a decrease in MMP-2 secretion. Our results show a complex pattern of regulation of ECM protein deposition by cAMP-mobilizing agents and also indicate an inverse correlation between ECM protein deposition and secretion of MMP-2. The concerted regulation of both of these processes is essential in the formation of new blood vessels, and for the integrity of the vascular wall.
机译：我们以前曾报道过，将培养的大鼠肾上腺髓质内皮细胞（RAMEC）短期暴露于凝血酶会增强细胞外基质（ECM）蛋白纤连蛋白，层粘连蛋白和I型（CI）和IV型（C-IV）胶原的内皮下沉积（ Papadimitriou等，1997）。在这项工作中，我们将对影响ECM蛋白沉积的因素的先前研究扩展到包括激活或抑制某些最常见的细胞内信号（例如cAMP，蛋白激酶C（PKC）和钙）的物质。此外，我们调查了观察到的ECM蛋白沉积变化与基质金属蛋白酶-2（MMP-2）分泌之间的可能联系。 Forskolin（腺苷酸环化酶激活剂）导致所研究的所有四种ECM蛋白的沉积呈剂量依赖性增加。异丙肾上腺素β-肾上腺素能受体激动剂）和膜渗透性cAMP类似物二丁酰-cAMP在低浓度下显着增加了ECM蛋白的沉积量，在两种药物的较高浓度下，这种增加都被逆转了。所有这些试剂对MMP-2的分泌都有相反的作用，在降低ECM蛋白沉积的剂量下增加了MMP-2的分泌，反之亦然。但是，磷酸二酯酶抑制剂IBMX升高cAMP对所研究的任何ECM蛋白的沉积量或MMP-2分泌均无影响。佛波酯（PMA）激活PKC导致ECM蛋白沉积减少，MMP-2分泌增加。最后，细胞间钙与BAPTA-AM的螯合导致ECM沉积增加，MMP-2分泌减少。我们的结果显示了通过cAMP动员剂调节ECM蛋白沉积的复杂模式，并且还表明ECM蛋白沉积与MMP-2分泌之间呈负相关。这两个过程的协调调节对于新血管的形成以及血管壁的完整性至关重要。

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