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Activation of Rac1-dependent redox signaling is critically involved in staurosporine-induced neurite outgrowth in PC12 cells

Title
Activation of Rac1-dependent redox signaling is critically involved in staurosporine-induced neurite outgrowth in PC12 cells
Authors
Kim, Du SikAn, Jeong MiLee, Han GilSeo, Su RyeonKim, Seon SookKim, Ju YeonKang, Jeong WanBae, Yun SooSeo, Jeong Taeg
Ewha Authors
배윤수
SCOPUS Author ID
배윤수scopus
Issue Date
2013
Journal Title
FREE RADICAL RESEARCH
ISSN
1071-5762JCR Link
Citation
vol. 47, no. 2, pp. 95 - 103
Keywords
staurosporineRac1reactive oxygen speciesneurite outgrowthPC12 cells
Publisher
INFORMA HEALTHCARE
Indexed
SCI; SCIE; SCOPUS WOS
Abstract
Staurosporine, a non-specific protein kinase inhibitor, has been shown to induce neurite outgrowth in PC12 cells, but the mechanism by which staurosporine induces neurite outgrowth is still obscure. In the present study, we investigated whether the activation of Rac1 was responsible for the neurite outgrowth triggered by staurosporine. Staurosporine caused rapid neurite outgrowth independent of the ERK signaling pathways. In contrast, neurite outgrowth in response to staurosporine was accompanied by activation of Rac1, and the Rac1 inhibitor NSC23766 attenuated the staurosporine-induced neurite outgrowth in a concentration-dependent manner. In addition, suppression of Rac1 activity by expression of the dominant negative mutant Rac1N17 also blocked the staurosporine-induced morphological differentiation of PC12 cells. Staurosporine caused an activation of NADPH oxidase and increased the production of reactive oxygen species (ROS), which was prevented by NSC23766 and diphenyleneiodonium (DPI), an NADPH oxidase inhibitor. Staurosporine-induced neurite outgrowth was attenuated by pretreatment with DPI and exogenous addition of sublethal concentration of H2O2 accelerated neurite outgrowth triggered by staurosporine. These results indicate that activation of Rac1, which leads to ROS generation, is required for neurite outgrowth induced by staurosporine in PC12 cells.
DOI
10.3109/10715762.2012.748193
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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