Receptor for advanced glycation end products activation injures primary sensory neurons via oxidative stress.

Receptor for advanced glycation end products activation injures primary sensory neurons via oxidative stress. Research Abstract Details 

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Receptor for advanced glycation end products activation injures primary sensory neurons via oxidative stress. Abstract Text:

Andrea M Vincent,Lorena Perrone,Kelli A Sullivan,Carey Backus,Ann Marie Sastry,Christian Lastoskie,Eva L Feldman,

The receptor for advanced glycation end products (RAGE) may promote diabetic vascular and renal disease through the activation of intracellular signaling pathways that promote oxidative stress. Oxidative stress is a mediator of hyperglycemia-induced cell injury and a unifying theme for all mechanisms of diabetic complications, but there are few studies on the expression and potential contribution of RAGE in diabetic neuropathy. The current study demonstrates that dorsal root ganglia neurons express functional RAGE and respond to the RAGE ligand S100 with similar downstream signaling, oxidative stress, and cellular injury as other diabetic complication-prone tissues. RAGE-induced phosphatidylinositol-3 kinase activity is associated with formation of reactive oxygen species, caspase-3 activation, and nuclear DNA degradation. These events are prevented by treatment with the antioxidant alpha-lipoic acid. Our data indicate that therapies aimed at decreasing RAGE ligands, blocking RAGE signaling, or preventing oxidative stress could significantly decrease the development of neuropathy in diabetic patients.

Receptor for advanced glycation end products activation injures primary sensory neurons via oxidative stress. Publishing Authors By Initials

AM Vincent,L Perrone,KA Sullivan,C Backus,AM Sastry,C Lastoskie,EL Feldman,

For similar biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research abstracts see: biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research

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Receptor for advanced glycation end products activation injures primary sensory neurons via oxidative stress. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Endocrinology

VOLUME: 148

Page Numbers: 548-58

Journal Abbreviation: Endocrinology

ISSN: 0013-7227

DAY: 9

MONTH: 11

YEAR: 2006

Receptor for advanced glycation end products activation injures primary sensory neurons via oxidative stress. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 375040

Receptor for advanced glycation end products activation injures primary sensory neurons via oxidative stress. Keywords Mesh Terms:

KEYWORDS: Signal Transduction

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Receptor for advanced glycation end products activation injures primary sensory neurons via oxidative stress. Information

Substance Name: Proto-Oncogene Proteins c-akt

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Receptor for advanced glycation end products activation injures primary sensory neurons via oxidative stress.

AFFILIATION: Department of Neurology, Room 5017 BSRB, University of Michigan, 109 Zina Pitcher Place, Ann Arbor, Michigan 48109, USA. andreav@umich.edu

Country: United States

AGENCY: United States NINDS

GRANT: NS38849

ACRONYM: NS

MEDLINETA: Endocrinology

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