期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 224, 期 3, 页码 786-794出版社
WILEY
DOI: 10.1002/jcp.22184
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资金
- Ministry of Education, Science and Technology of Korea through the National Research Foundation of Korea [NRF] [R13-2005-022-03001-0]
- National Research Foundation of Korea [R13-2005-022-03001-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
The rat pheochromocytoma cell line PCI2 has been widely used as a model to study neuronal differentiation. PCI2 cells give rise to neurites in response to basic fibroblast growth factor (bFGF). However, it is unclear whether bFGF promotes neurite outgrowth by inducing RhoA inactivation, and a mechanism for RhoA inactivation in PCI2 cells in response to bFGF has not been reported. Lysophosphatidic acid (LPA) treatment and the expression of constitutively active (CA)-RhoA (RhoA VI 4) impaired neurite formation in response to bFGF, while Tat-C3 exoenzyme and the expression of dominant negative (DN)-RhoA (RhoA NI 9) stimulated neurite outgrowth. GTP-bound RhoA levels were reduced in response to bFGF, which suggests that the inactivation of RhoA is essential to neurite outgrowth in response to bFGF. To investigate the mechanism of RhoA inactivation, this study examined the roles of p190RhoGAP and Rap-dependent RhoGAP (ARAP3). DN-p190RhoGAP prevented neurite outgrowth, while WT-p190RhoGAP and Src synergistically stimulated neurite outgrowth; these findings suggest that bFGF promotes the inactivation of RhoA and subsequent neurite outgrowth through p190RhoGAP and Src. Furthermore, DN-RapI and DN-ARAP3 reduced neurite formation in PCI2 cells. These results suggest that RhoA is likely to be inactivated by p190RhoGAP and ARAP3 during neurite outgrowth in response to bFGF. J. Cell. Physiol. 224: 786-794, 2010. (C) 2010 Wiley-Liss, Inc.
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