期刊
CELLULAR SIGNALLING
卷 26, 期 2, 页码 220-232出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2013.10.010
关键词
Tissue kallikrein; Neurite outgrowth; Epidermal growth factor receptor; Flotillin-2; Extracellular signal-regulated kinase
类别
资金
- National Natural Science Foundation of China [81271295, 81000487]
Tissue kallikrein (TK) was previously shown to take most of its biological effects through bradykinin receptors. In this study, we assumed that TK mediated neurite outgrowth was independent of bradykinin receptors. To test the hypothesis, we investigated TK-induced neurite outgrowth and its signaling mechanisms in cultured primary neurons and human SH-SY5Y cells. We found that TIC stimulation could increase the number of processes and mean process length of primary neurons, which were blocked by epidermal growth factor receptor (EGFR) inhibitor or down-regulation, small interfering RNA for flotillin-2 and extracellular signal-regulated kinase (ERK) 1/2 inhibitor. Moreover, TIC-induced neurite outgrowth was associated with EGFR and ERK1/2 activation, which were inhibited by EGFR antagonist or RNA interference and flotillin-2 knockdown. Interestingly, inhibition of bradykinin receptors had no significant effects on EGFR and ERK1/2 phosphorylation. In the present research, our data also suggested that EGFR and flotillin-2 formed constitutive complex that translocated to around the nuclei in the TIC stimulation. In sum, our findings provided evidence that TIC could promote neurite outgrowth via EGFR, flotillin-2 and ERK1/2 signaling pathway in vitro. (C) 2013 Elsevier Inc. All rights reserved.
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