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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Age Factors, Analysis of Variance, Animals, Blood Glucose, Caspase 3, Diabetes Mellitus, Experimental, Disease Models, Animal, Female, Ganglia, Spinal, Gene Expression Regulation, Glycated Hemoglobin A, HSP27 Heat-Shock Proteins, Humans, Hyperalgesia, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Mitogen-Activated Protein Kinases, Nerve Fibers, Neural Conduction, Pain Threshold, Peripheral Nerves, Protein-Serine-Threonine Kinases, Sensory Receptor Cells, Signal Transduction, Skin, Streptozocin, Time Factors.
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Does overexpression of human HSP27 protect sensory neurons from diabetes? Context: To evaluate whether augmenting neuronal protective mechanisms might slow or arrest experimental diabetic peripheral neuropathy (DPN). DPN is one of the most common neurodegenerative disorders and is rising in prevalence. How it targets sensory neurons is uncertain; the disorder is irreversible and untreatable. We explored the intrinsic protective properties of overexpressed human HSP27 on experimental DPN. HSP27 is a small pro-survival heat shock protein that also increases axonal regeneration. Experimental diabetes was superimposed on mice overexpressing a human HSP27 transgene and its impact was evaluated on epidermal innervation, behavioral tests of sensation and electrophysiological indices of DPN. Mice that overexpress human HSP27 in their sensory and motor neurons and that were made diabetic for 6 months by streptozotocin treatment were protected from a range of neuropathic abnormalities, including loss of footpad thermal sensation, mechanical allodynia, loss of epidermal innervation, and slowing of sensory conduction velocity. The protection was selective for sensory neurons in comparison to motor neurons and at 6 months provided better protection in female than male mice. Markers of RAGE-NFκB activation were attenuated by the transgene.
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The findings support the idea that diabetic polyneuropathy involves a unique, sensory-centric neurodegenerative process which can be reduced by overexpressing a single gene, an important starting point for new disease-modifying therapeutic approaches. Final Decision: yes