STZ causes depletion of immune cells in sciatic nerve and dorsal root ganglion in experimental diabetes

Streptozotocin (STZ) treatment, a common model for inducing diabetes in rodent models, induces thermal hyperalgesia and neuronal toxicity independently of hyperglycemia by oxidizing and activating TRPA1 and TRPV1. Following treatment with STZ, CD45+ immune cells were found to be depleted in sciatic...

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Bibliographic Details
Main Authors: Hidmark, Asa S. (Author) , Nawroth, Peter Paul (Author) , Fleming, Thomas (Author)
Format: Article (Journal)
Language:English
Published: 2017
In: Journal of neuroimmunology
Year: 2017, Volume: 306, Pages: 76-82
ISSN:1872-8421
DOI:10.1016/j.jneuroim.2017.03.008
Online Access:Verlag, Volltext: http://dx.doi.org/10.1016/j.jneuroim.2017.03.008
Verlag, Volltext: http://www.sciencedirect.com/science/article/pii/S016557281630248X
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Author Notes:Asa S. Hidmark, Peter P. Nawroth, Thomas Fleming
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Summary:Streptozotocin (STZ) treatment, a common model for inducing diabetes in rodent models, induces thermal hyperalgesia and neuronal toxicity independently of hyperglycemia by oxidizing and activating TRPA1 and TRPV1. Following treatment with STZ, CD45+ immune cells were found to be depleted in sciatic nerve (SN) and DRG in mice, prior to hyperglycemia. Macrophages were also lost in DRG and NFκB-p65-activation was increased in SN macrophages. Immune cells were significantly reduced in both SN and DRG up to three weeks, post-treatment. Loss of PNS-resident macrophages in response to STZ-mediated toxicity may affect the regenerative capacity of the nerve in response to further injury caused by diabetes.
Item Description:Available online 11 March 2017
Gesehen am 15.06.2018
Physical Description:Online Resource
ISSN:1872-8421
DOI:10.1016/j.jneuroim.2017.03.008