TrkB-T1 regulates the RhoA signaling and actin cytoskeleton in glioma cells
TrkB-T1 regulates the RhoA signaling and actin cytoskeleton in glioma cells
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DOI：
10.1016/j.bbrc.2006.02.033
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发表时间：
2006-04-14
影响因子：
3.1
通讯作者：
Hayashi, M
中科院分区：
文献类型：
--
作者：
Ohira, K;Homma, KJ;Hayashi, M
最近，截短的TrkB受体，T1，已被报道参与通过调节Rho蛋白的细胞形态的控制，通过该T1结合Rho鸟嘌呤核苷酸解离抑制剂（Rho GDI）1，并以脑源性神经营养因子（BIDNIF）依赖的方式将其解离。然而，目前还不清楚T1信号是否调节下游的Rho信号和肌动蛋白细胞骨架。在这项研究中，我们研究了这个问题，使用C6大鼠胶质瘤细胞，内源性表达T1。Rho GDI I以BDNF依赖的方式从T1解离，这也导致Rho信号分子如RhoA、Rho相关激酶、p21激活激酶和细胞外信号调节激酶1/2的活性降低。此外，BDNF治疗导致在与溶血磷脂酸，Rho的激活剂处理的细胞中的应力纤维的消失，并在细胞的形态学变化。此外，与T1特异性序列的青色荧光蛋白融合蛋白的竞争性测定降低了BDNF的作用。这些结果表明，T1调节Rho信号通路和肌动蛋白细胞骨架。(c)2006年爱思唯尔公司All rights reserved.
Recently, the truncated TrkB receptor, T1, has been reported to be involved in the control of cell morphology via the regulation of Rho proteins, through which T1 binds Rho guanine nucleotide dissociation inhibitor (Rho GDI) 1 and dissociates it in a brain-derived neurotrophic factor (BIDNIF)-dependent manner. However, it is unclear whether T1 signaling regulates the downstream of Rho signaling and the actin cytoskeleton. In this study, we investigated this question using C6 rat glioma cells, which express T1 endogenously. Rho GDI I was dissociated from T1 in a BDNF-dependent manner, which also causes decreases in the activities of Rho-signaling molecules such as RhoA, Rho-associated kinase, p21-activated kinase, and extracellular-signal regulated kinase1/2. Moreover, BDNF treatment resulted in the disappearance of stress fibers in the cells treated with lysophosphatidic acid, an activator of Rho& and in morphological changes in cells. Furthermore, a competitive assay with cyan fluorescent protein fusion proteins of T1-specific sequences reduced the effects of BDNF. These results suggest that T1 regulates the Rho-signaling pathways and the actin cytoskeleton. (c) 2006 Elsevier Inc. All rights reserved.