Naslov
A role of calcium/calmodulin-dependent protein kinase II (CaMKII) in diabetic neuropathy

Autori
Ferhatović, Lejla ; Kostić, Sandra ; Banožić, Adriana ; Vrdoljak, Luka ; Sapunar, Damir ; Puljak, Livia

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Skup
Bridges in Life Sciences 7th Annual Conference: Science and Art for the Advancement of Medicine, Budapest, Hungary

Mjesto i datum
Budimpešta, Mađarska, 30.03.2012. - 01.04.2012

Vrsta sudjelovanja
Predavanje

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
diabetic neuropathy; diabetes type 1; diabetes type 2; pain; CaMKII

Sažetak
AIMS: Abnormalities in peripheral nerve and dorsal root ganglion (DRG) have been noted in early stages of experimentally-induced diabetes. The enzyme calcium/calmodulin-dependent protein kinase II (CaMKII) has been linked with neuropathic pain. The aim of this study was to compare expression of total CaMKII (tCaMKII) and its phosphorilated alpha isoform (pCaMKII-alpha) in rat models of diabets mellitus type 1 (DM1) and II (DM2), as well as their pain-related behavior. METHODS: Sprague-Dawley rats were injected with streptozotocin to get DM1, while DM2 was induced with combination of high-fat diet and low-doze streptozotocin. Pain-related behavior was analyzed with thermal and mechanical stimuli. On the 14th post-injection day, rats were sacrificed and DRGs were sectioned. For detection of tCaMKII and pCaMKII-alpha, immunofluorescence was used and measured with Metamorph software. RESULTS: Comparison between DM1 and control rats revealed significant difference following cold stimuli. In DM2 control group we saw increase in pain responsiveness following thermal (cold) and mechanical stimuli, comparing to DM2 group. In DM1 rats we observed significant difference between control and diabetic rats in tCaMKII expression, while this difference was not observed in DM2 model. In both DM models pCaMKII-alpha expression was increased. CONCLUSIONS: Differences in pain-related behavior were observed in rat diabetes models after only two weeks. Experimetnaly-induced diabetes increases expression of tCaMKII (in DM1) and pCaMKII-alpha (DM1 and 2) in sensory neurons. This may indicate involvement of this enzyme in tramsission of nociceptive input early in diabetes. CaMKII may be a suitable pharmacological target for diabetic neuropathy. The experiments are continued in DM1 and DM2 rats that will live for 2 months, 6 months and 12 months.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

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