Cunningham D D, Gurwitz D
Department of Microbiology and Molecular Genetics, College of Medicine, University of California, Irvine 92717.
J Cell Biochem. 1989 Jan;39(1):55-64. doi: 10.1002/jcb.240390107.
This review summarizes studies on the reciprocal regulation of neuroblastoma neurite outgrowth by thrombin and protease nexin-1 (PN-1). PN-1 recently was shown to possess the same deduced amino acid sequence as the glial-derived neurite-promoting factor. The neurite outgrowth activity of PN-1 depends on its ability to inhibit thrombin. Thrombin not only blocks the neurite outgrowth activity of PN-1, but it also brings about neurite retraction in the presence of PN-1. Thrombin also produces neurite retraction in the absence of PN-1 and other regulatory factors. This suggests that its activity is due to a direct action on cells. The neurite retraction by thrombin depends on its proteolytic activity. It does not occur with the other serine proteases that have been tested, indicating that it is a specific effect and is not due to a general proteolytic effect that could detach neurites from the culture dish. Serum brings about neurite retraction in certain neuroblastoma cells and primary neuronal cultures; most of this activity is due to residual thrombin in the serum. Together, these results suggest that PN-1 and thrombin (or a thrombin-like protease) play a role in regulation of neurite outgrowth.
本综述总结了关于凝血酶和蛋白酶连接素-1(PN-1)对神经母细胞瘤神经突生长的相互调节作用的研究。最近发现PN-1与神经胶质衍生的神经突促进因子具有相同的推导氨基酸序列。PN-1的神经突生长活性取决于其抑制凝血酶的能力。凝血酶不仅会阻断PN-1的神经突生长活性,而且在有PN-1存在的情况下还会导致神经突回缩。在没有PN-1和其他调节因子的情况下,凝血酶也会引起神经突回缩。这表明其活性是由于对细胞的直接作用。凝血酶引起的神经突回缩取决于其蛋白水解活性。在已测试的其他丝氨酸蛋白酶中不会出现这种情况,这表明这是一种特异性作用,并非由于可能使神经突从培养皿上脱离的一般蛋白水解作用。血清会在某些神经母细胞瘤细胞和原代神经元培养物中引起神经突回缩;这种活性大部分归因于血清中残留的凝血酶。总之,这些结果表明PN-1和凝血酶(或一种凝血酶样蛋白酶)在神经突生长的调节中起作用。