PKCδ splicing variant (PKCδIII) induces neurite outgrowth in PC12 cells in the absence of NGF

Abstract

AbstractProtein kinase C (PKC)δ is a serine/threonine kinase involved in many cellular processes in response to diverse stimuli, including cell proliferation, differentiation, apoptosis, tumor inhibition, and cell migration. PKCδ consists of the N terminal regulatory domain and the C terminal catalytic domain, which are linked with a hinge region. An alternative splicing variant of rat PKCδ (also known as PKCδIII) has been reported, and this PKCδ splicing variant (SV) has only the regulatory domain without the catalytic domain. However, its function remains unclear. In this study, we found that PKCδ SV induced neurite outgrowth in the absence of nerve growth factor (NGF) in PC12 cells. Immunoblot analysis revealed that ERK was phosphorylated by NGF treatment, but not by PKCδ SV induction, indicating that PKCδ SV-mediated neurite outgrowth was different from NGF-mediated one. In addition, we showed that PKCδ full length and SV increased their mRNA expression after NGF treatment and that PKCδ SV was more susceptible to its proteasomal degradation. Our findings provided insights into the role of PKCδSV in neurite outgrowth.