| First Author | Ohkawa Y | Year | 2011 |
| Journal | Biochem Biophys Res Commun | Volume | 411 |
| Issue | 3 | Pages | 483-9 |
| PubMed ID | 21723256 | Mgi Jnum | J:175700 |
| Mgi Id | MGI:5287061 | Doi | 10.1016/j.bbrc.2011.06.118 |
| Citation | Ohkawa Y, et al. (2011) Wisp2/CCN5 up-regulated in the central nervous system of GM3-only mice facilitates neurite formation in Neuro2a cells via integrin-Akt signaling. Biochem Biophys Res Commun 411(3):483-9 |
| abstractText | Wisp2/CCN5 belongs to CCN family proteins which are involved in cell proliferation, angiogenesis, tumorigenesis and wound healing. Although a number of studies on the roles of Wisp2/CCN5 in cancers have been reported, no study on the expression and function of Wisp2/CCN5 in the central nervous system has been reported. In this study, we focused on Wisp2/CCN5 that was up-regulated in nervous tissues in GM3-only mice. Over-expression of Wisp2/CCN5 enhanced neurite outgrowth potently after serum withdrawal with increased phosphorylation levels of Akt and ERKs. When cells were cultured with recombinant Wisp2/CCN5 proteins, more and longer neurites were formed than in the controls. Thus, we demonstrated for the first time that Wisp2/CCN5 facilitates neurite formation in a mouse neuroblastoma cell line, Neuro2a. Akt phosphorylation induced by recombinant Wisp2/CCN5 was suppressed after knockdown of integrin beta1. Moreover, Wisp2/CCN5-over-expressing cells were resistant to apoptosis induced by H(2)O(2). These results suggested that secreted Wisp2/CCN5 induces Akt and ERK phosphorylation via integrins, and consequently facilitates neurite formation and conferred resistance to apoptosis. Up-regulation of Wisp2/CCN5 in GM3-only mice should be, therefore, a reaction to protect nervous tissues from neurodegeneration caused by ganglioside deficiency. |
