Article ID Journal Published Year Pages File Type
2590088 NeuroToxicology 2009 6 Pages PDF
Abstract

Previous studies have shown that apoptosis can be mediated by activation of either calmodulin kinase II (CaMKII) or mitogen-activated protein kinase (MAPK), ERK and p38. In the present study, we investigated whether CaMKII is involved in activation of ERK and p38 in response to all-trans retinoic acid (ATRA) treatment in PC12 cells. Results showed that ATRA-induced activation of ERK and p38 occurred later than that of CAMKII. Knockdown of CAMKII by siRNA significantly suppressed ATRA-induced activation of ERK and p38. These results demonstrated that activation of ERK and p38 following ATRA exposure is CAMKII-dependent. Treatment with ATRA also resulted in cell death characterized by apoptosis in PC12 cells. Results suggest that CaMKII-dependent activation of ERK and p38 is related to apoptotic cell death.

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