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A role for mitogen-activated protein kinases in the etiology of diabetic neuropathy.

Purves T, Middlemas A, Agthong S, Jude E, Boulton AJM, Fernyhough P, Tomlinson D

FASEB J. 2001;15( 13):2508-14.

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Abstract

The onset of diabetic neuropathy, a complication of diabetes mellitus, has been linked to poor glycemic control. We tested the hypothesis that the mitogen-activated protein kinases (MAPK) form transducers for the damaging effects of high glucose. In cultures of adult rat sensory neurons, high glucose activated JNK and p38 MAPK but did not result in cell damage. However, oxidative stress activated ERK and p38 MAPKs and resulted in cellular damage. In the dorsal root ganglia of streptozotocin-induced diabetic rats (a model of type I diabetes), ERK and p38 were activated at 8 wk duration, followed by activation of JNK at 12 wk duration. We report activation of JNK and increases in total levels of p38 and JNK in sural nerve of type I and II diabetic patients. These data implicate MAPKs in the etiology of diabetic neuropathy both via direct effects of glucose and via glucose-induced oxidative stress.

Bibliographic metadata

Type of resource:
Content type:
Publication type:
Published date:
Journal title:
ISSN:
Place of publication:
United States
Volume:
15( 13)
Start page:
2508
End page:
14
Pagination:
2508-14
Access state:
Active

Institutional metadata

University researcher(s):

Record metadata

Manchester eScholar ID:
uk-ac-man-scw:1d29741
Created:
2nd September, 2009, 12:00:52
Last modified:
14th August, 2012, 07:10:20

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