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首页> 外文期刊>Journal of Cellular Physiology >Independent regulation of matrix metalloproteinases and plasminogen activators in human fibrosarcoma cells.
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Independent regulation of matrix metalloproteinases and plasminogen activators in human fibrosarcoma cells.

机译：独立的监管矩阵金属蛋白酶、纤溶酶原激活物物人类纤维肉瘤细胞。

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Serine proteases and matrix metalloproteinases have been shown to often cooperate in multiple physiological and pathological processes associated with changes in the extracellular matrix (ECM). We have examined the interaction between the plasminogen activator (PA)-plasmin system and matrix metalloproteinases (MMPs) in HT1080 human fibrosarcoma cells treated with 12-O-tetradecanoyl-phorbol-13-acetate (TPA). While TPA treatment evoked a temporary increased expression of urokinase type PA (uPA), the production of both types of human plasminogen activator inhibitors (PAI) was induced and sustained over 12 h by TPA treatment shifting the protease-protease inhibitors balance in favor of the inhibitors. TPA treatment of HT1080 cells induced the expression of interstitial collagenase (MMP-1) and increased the expression of gelatinase B (MMP-9), tissue inhibitor of metalloproteinases-1 (TIMP-1), and MT-MMP, a membrane-bound activator of progelatinase A (proMMP-2), while MMP-2 and TIMP-2 expression were decreased. Increased MT-MMP expression by TPA treatment was associated with increased activation of proMMP-2. These data show that the regulation of PA-plasmin and metalloproteinase and their specific inhibitors is uncoordinated. In addition, inhibition of the PA-plasmin system by PAI-2 or aprotinin did not prevent the activation of proMMP-2 by TPA, suggesting that plasmin is not involved in MT-MMP-mediated activation of proMMP-2.
机译：丝氨酸蛋白酶和基质金属蛋白酶已被证明经常在多个合作吗生理和病理过程与细胞外的变化有关矩阵(ECM)。纤溶酶原激活物(PA)之间的胞浆素系统和基质金属蛋白酶(MMPs)HT1080人类纤维肉瘤细胞治疗12-O-tetradecanoyl-phorbol-13-acetate (TPA)。虽然TPA治疗诱发一个临时增加尿激酶型PA (uPA)的表达式生产两种类型的人纤溶酶原。物诱导和激活抑制剂(PAI)持续超过12 h TPA治疗转移protease-protease抑制剂的平衡抑制剂。诱导间质性的表达胶原酶(金属蛋白酶- 1)和增加了的表情白明胶酶B (MMP-9),组织抑制剂metalloproteinases-1 (TIMP-1)和MT-MMP膜结合progelatinase的活化剂(proMMP-2),而MMP-2和TIMP-2表达式被降低了。TPA治疗与增加有关proMMP-2激活。监管PA-plasmin和金属蛋白酶和他们的特定抑制剂不协调。此外,抑制PA-plasmin系统通过PAI-2或抑肽酶并没有阻止激活的proMMP-2 TPA,暗示血纤维蛋白溶酶没有参与MT-MMP-mediatedproMMP-2激活。

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