Diabetes impairs an interleukin-1[beta]-dependent pathway that enhances neurite outgrowth through JAK/STAT3 modulation of mitochondrial bioenergetics in adult sensory neurons

Background A luminex-based screen of cytokine expression in dorsal root ganglia (DRG) and nerve of type 1 diabetic rodents revealed interleukin-1 (IL-1[alpha]) and IL-1[beta] to be significantly depressed. We, therefore, tested the hypothesis that impaired IL-1[alpha] and IL-1[beta] expression in DR...

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Bibliographic Details
Published in:Molecular brain 2013-10, Vol.6 (1), p.45-45
Main Authors: Saleh, Ali, Roy Chowdhury, Subir K, Smith, Darrell R, Balakrishnan, Savitha, Tessler, Lori, Schartner, Emily, Bilodeau, Andre, Van Der Ploeg, Randy, Fernyhough, Paul
Format: Article
Language:English
Subjects:
Axonogenesis
Cellular control mechanisms
Colleges & universities
Cytokines
Diabetes
Diabetic neuropathies
Diabetic neuropathy
Experiments
Health aspects
Interleukin-1
Medical research
Mitochondria
Neurons
Phosphorylation
Physiological aspects
Proteins
Rodents
Sensory receptors
Software
Streptozocin
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Summary:Background A luminex-based screen of cytokine expression in dorsal root ganglia (DRG) and nerve of type 1 diabetic rodents revealed interleukin-1 (IL-1[alpha]) and IL-1[beta] to be significantly depressed. We, therefore, tested the hypothesis that impaired IL-1[alpha] and IL-1[beta] expression in DRG may contribute to aberrant axon regeneration and plasticity seen in diabetic sensory neuropathy. In addition, we determined if these cytokines could optimize mitochondrial bioenergetics since mitochondrial dysfunction is a key etiological factor in diabetic neuropathy. Results Cytokines IL-1[alpha] and IL-1[beta] were reduced 2-fold (p
ISSN:1756-6606
1756-6606
DOI:10.1186/1756-6606-6-45