Expression of axotomy-inducible and apoptosis-related genes in sensory nerves of rats with experimental diabetes

R. C. Burnand, S. A. Price, M. McElhaney, D. Barker, D. R. Tomlinson

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    In diabetes, peripheral nerves suffer deficient neurotrophic support - a situation which resembles axotomy. This raises the question: does inappropriate establishment of an axotomised neuronal phenotype contribute to diabetic neuropathy, and in extremis, does this provoke apoptosis? We hybridized reverse-transcribed RNA, from the dorsal root ganglia (DRG) of 8-week streptozotocin (STZ)-induced diabetic rats, to Affymetrix Rat Genome U34A chips and scanned the array for expression of (a) genes that are upregulated by axotomy, (b) proapoptotic and (c) anti-apoptotic genes. Expression of the axotomy-responsive genes coding for growth-associated protein 43 (GAP-43), galanin, neuropeptide Y (NPY), pre-pro-vasoactive intestinal polypeptide (pre-pro-VIP), neuronal nitric oxide synthase (nNOS), protease nexin 1, heat-shock protein 27 (HSP 27) and myosin light chain kinase II (MLCK II) was unaffected in ganglia from diabetic rats compared to controls; thus, no axotomised phenotype was established. The expression of the majority of proapoptotic genes in the DRG was also unaltered (bax, bad, bid, bok, c-Jun, p38, TNFR1, caspase 3 and NOS2). Similarly there was no change in expression of the majority of antiapoptotic genes (bcl2, bcl-xL, bcl-w, NfkappaB). These alterations in gene expression make it clear that neither axotomy nor apoptotic phenotypes are established in neurones in this model of diabetes. © 2004 Elsevier B.V. All rights reserved.
    Original languageEnglish
    Pages (from-to)235-240
    Number of pages5
    JournalMolecular Brain Research
    Issue number2
    Publication statusPublished - 20 Dec 2004


    • Apoptosis
    • Axotomy
    • Degenerative disease: other
    • Disorders of the nervous system
    • Gene expression
    • Neuropathy
    • Sensory neurones


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