Expression of calcium/calmodulin-dependent protein kinase II in dorsal root ganglia in diabetic rats 6 months and 1 year after diabetes induction

Abstract

Aim The aim of this study was to compare expression of total calcium/calmodulin-dependent protein kinase II (tCaMKII) and its α, β, γ and δ isoforms in dorsal root ganglion (DRG) in rat models of diabetes mellitus type I (DM1), 6 months and 1 year after diabetes induction. Methods A total of 45 male Sprague-Dawley rats weighing 160-200 g were assigned into four experimental groups: 6-months DM1 and its control group, 1-year and its control group. For the induction of DM1, after overnight fasting animals were injected intraperitonealy with 55 mg/kg of the streptozotocine (STZ). Rats were sacrificed 6 months and 1 year after the diabetes induction. The L4 and L5 ganglions were removed, fixed, embedded in freezing medium and sectioned on a cryostat. Immunofluorescence analysis was performed for detection of tCaMKII and its α, β, γ and δ isoforms. Image J software was used for analysis of immunofluorescence. Results The diabetes was successfully induced as confirmed by measurement of glucose levels and weight increase. Analysis of tCaMKII expression in DRGs revealed no differences between DM1 and control animals after 6 and 12 months. In diabetic animals, the expression of α and β isoforms decreased significantly after 6 months, compared to the controls, while decrease of γ and δ was observed after one year of diabetes in diabetic animals. Conclusions The observed changes in the expression of CaMKII isoforms reveal plastic changes of this enzyme during the chronic diabetic state and may be involved in the chronic neuropathic pain development.

The functions of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in diabetes progression

“…However, work by Ferhatovic et al (2014) suggested that the decrease of CaMKII in the dorsal root ganglia in long-term diabetes is responsible for developing neuropathy and increased neuropathic pain (Ferhatovic et al 2014). CaMKII is involved in ERK activation and thus plays a role in neuropathic pain induction.…”