Diabetic Peripheral Neuropathy (DPN) manifests in 60% of diabetic patients and counts for one of the major causes of peripheral members amputation. Besides, diabetes is responsible for 30% of all neuropathic pain diagnosed. Even though the electrophysiological and morphological aspects are well described, little is known about its development and progression, impossibilitating effective therapies. It is believed that hyperglycemia and insulin impairment signaling are the main events behind oxidative stress observed in nerves. Several hypothesis try to explain the phenomenon, like enhancement activity of the polliol pathway, greater production of AGES, impairment of neurotrofic support, PKC activity enhancement and mitochondrial failure, but until now there are still many gaps in the disease development knowledge and the cellular populations involved. Besides neurons, there are evidences that glial satellite cell located in the dorsal root ganglia (DRG) actively contribute to inflammation promotion in injury neuropathy, a non-explored fact in DPN. Recent data from our laboratory correlate experimentally DPN development with a shorter period in developing hyperglycemia induced by low doses of streptozotocin (STZ) whether late hyperglycemic rats in the same model did not had DPN. These original data permitted us to establish new model criteria of diabetes induced by STZ more close to the clinic. That said, this project objective is to explore, by DNA microarrays analysis, the major molecules or pathways differentially expressed in neurons and glial satellite cells of DRG from rats model of STZ-induced type I diabetes presenting DPN or not. Further, the possible candidate genes will be validated in the same tissues, by Real-Time PCR and Western Blot. With this approach we expect to find potential genes or pathways that might be enrolled with, allowing future advances in effective treatments or even neuropatic reversion.
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