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Amelioration of retarded neurite outgrowth of dorsal root ganglion neurons by overexpression of PKC&dgr; in diabetic rats

To examine which isoform of protein kinase C (PKC) may be associated with impaired nerve regeneration in diabetes, we compared neurite outgrowth of isolated dorsal root ganglion (DRG) neurons in streptozocin (STZ)-induced diabetic and control rats. Neurite outgrowth was significantly retarded in diabetic neurons. Rottlerin, a PKC&dgr; specific inhibitor, significantly retracted neurite outgrowth whereas Gö6976, an inhibitor specific for classical PKCs, had no effect, suggesting a significant role of PKC&dgr; in neurite outgrowth of DRG neurons. The expression of phosphorylated PKC&dgr;, but not total PKC&dgr;, in DRGs was decreased in diabetic rats. When this reduced expression was restored by overexpressing the PKC&dgr; in isolated DRG neurons, retardation of neurite outgrowth was significantly reversed in diabetic rats. These results suggest that a decrease in phosphorylated PKC&dgr; is at least in part responsible for impaired neurite outgrowth in diabetes, and that PKC&dgr; plays a significant role in the pathogenesis of diabetic neuropathy. This observation provides a useful clue for the treatment of diabetic neuropathy.