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Hidmark, A.S.* ; Nawroth, P.P. ; Fleming, T.*

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

J. Neuroimmunol. 306, 76-82 (2017)
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Diabetic Neuropathy ; Experimental Diabetes ; Macrophage ; Neurotoxicity; Thermal Hyperalgesia; Scavenger-receptor; Sensitive Method; Spinal-cord; Streptozotocin; Macrophages; Neuropathy; Pain; Regeneration; Expression
ISSN (print) / ISBN 0165-5728
e-ISSN 1872-8421
Quellenangaben Band: 306, Heft: , Seiten: 76-82 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort Amsterdam
Begutachtungsstatus Peer reviewed