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SOD2 Protects Neurons from Injury in Cell Culture and Animal Models of Diabetic
Andrea M. Vincent, James W. Russell, Kelli A. Sullivan, Carey Backus, John M.
Hayes, Lisa L. McLean and Eva L. Feldman
Eva Feldman on 9/19/2007
Volume : Pages
208 : 216 - 227
Hyperglycemia-induced oxidative stress is an inciting event in the development
of diabetic complications including diabetic neuropathy. Our observations of
significant oxidative stress and morphological abnormalities in mitochondria led
us to examine manganese superoxide dismutase (SOD2), the enzyme responsible for
mitochondrial detoxification of oxygen radicals. We demonstrate that over
expression of SOD2 decreases superoxide (O2.-) in cultured primary dorsal root
ganglion (DRG) neurons and subsequently blocks caspase-3 activation and cellular
injury. Under expression of SOD2 in dissociated DRG cultures from adult SOD2+/-
mice results in increased levels of O2.-, activation of caspase-3 cleavage and
decreased neurite outgrowth under basal conditions that are exacerbated by
hyperglycemia. These profound changes in sensory neurons led us to explore the
effects of decreased SOD2 on the development of diabetic neuropathy (DN) in
mice. DN was assessed in SOD2+/- C57BL/6J mice and their SOD2+/+ litter mates
following streptozotocin (STZ) treatment. These animals, while hyperglycemic, do
not display any signs of DN. DN was observed in the C57BL/6Jdb/db mouse, and
decreased expression of SOD2 in these animals increased DN. Our data suggest
that SOD2 activity is an important cellular modifier of neuronal oxidative
defense against hyperglycemic injury.
Investigators with authorship
University of Michigan
Neuropathy & Neurocognition
caspase 3, apoptosis related cysteine protease
superoxide dismutase 2, mitochondrial
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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