THROMBIN CAUSES NEURITE RETRACTION IN NEURONAL CELLS THROUGH ACTIVATION OF CELL-SURFACE RECEPTORS
THROMBIN CAUSES NEURITE RETRACTION IN NEURONAL CELLS THROUGH ACTIVATION OF CELL-SURFACE RECEPTORS
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DOI：
10.1016/0896-6273(92)90302-t
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发表时间：
1992-02-01
期刊：
影响因子：
16.2
通讯作者：
MONARD, D
中科院分区：
文献类型：
--
作者：
SUIDAN, HS;STONE, SR;MONARD, D
在 NB2a 小鼠神经母细胞瘤细胞中研究了凝血酶诱导神经突收缩的机制。凝血酶的快速作用（在几分钟内完成）似乎涉及其阴离子结合外位点和凝血酶受体之间的相互作用。该位点的结构改变会增加凝血酶介导的回缩的 EC50，而阻断该位点的水蛭素 C 端肽会抑制该反应。凝血酶效应通过从 Ser-42 开始的 14 个氨基酸肽来模拟，该肽位于人凝血酶受体的拟议切割位点。蛋白激酶抑制剂星形孢菌素和 H-7 可阻止凝血酶诱导的收缩。因此，提出凝血酶介导的神经突回缩是由凝血酶受体的裂解诱导的激活引起的，并且涉及蛋白激酶的刺激。
The mechanism by which thrombin induces neurite retraction was studied in NB2a mouse neuroblastoma cells. The rapid effect of thrombin (completed within minutes) appears to involve an interaction between its anion-binding exosite and the thrombin receptor. Structural alterations of this site increase the EC50 for thrombin-mediated retraction, and a hirudin C-terminal peptide that blocks this site inhibits the response. The thrombin effect was mimicked by a 14 amino acid peptide starting with Ser-42, at the proposed cleavage site of the human thrombin receptor. The protein kinase inhibitors staurosporine and H-7 blocked thrombin-induced retraction. It is therefore proposed that thrombin-mediated neurite retraction is caused by cleavage-induced activation of the thrombin receptor and involves stimulation of a protein kinase(s).