Neuronal RAGE expression modulates severity of injury following transient focal cerebral ischemia

Journal of Clinical Neuroscience

Volumn 16, Issue 2, 2009, Pages 302-306

  Hassid, Benjamin G ^a   Nair, M Nathan ^b   Ducruet, Andrew F ^a   Otten, Marc L ^a   Komotar, Ricardo J ^a   Pinsky, David J ^c   Schmidt, Ann Marie ^a   Yan, Shi Fang ^a   Connolly, E Sander ^a  

^a Och Spine at New York Presbyterian Hospitals   (United States)

^b UNIVERSITY OF WASHINGTON SCHOOL OF MEDICINE   (United States)

^c UNIVERSITY OF MICHIGAN MEDICAL SCHOOL   (United States)

Author keywords

Inflammation; Ischemia; Murine; RAGE; Reperfusion; Stroke

Indexed keywords

CYTOPLASMIC RECEPTOR; PROTEIN DERIVATIVE; PROTEIN RAGE; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN INJURY; CONTROLLED STUDY; DISEASE SEVERITY; GENE DELETION; GENE OVEREXPRESSION; IMMUNOHISTOCHEMISTRY; MALE; MOUSE; NERVE CELL; NONHUMAN; PRIORITY JOURNAL; PROTEIN DOMAIN; PROTEIN EXPRESSION; PROTEIN FUNCTION; SIGNAL TRANSDUCTION; STROKE; TRANSIENT ISCHEMIC ATTACK;

ANIMALS; DISEASE MODELS, ANIMAL; GENE EXPRESSION REGULATION; HUMANS; ISCHEMIC ATTACK, TRANSIENT; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; NEURONS; PROTEIN STRUCTURE, TERTIARY; RECEPTORS, IMMUNOLOGIC; SEVERITY OF ILLNESS INDEX;

EID: 58149187856     PISSN: 09675868     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.jocn.2007.12.011     Document Type: Article

References (17)

1. Kislinger T., Fu C., Huber B., et al. N(epsilon)-(carboxymethyl)lysine adducts of proteins are ligands for receptor for advanced glycation end products that activate cell signaling pathways and modulate gene expression. J Biol Chem 274 (1999) 31740-31749
2. Bucciarelli L.G., Kaneko M., Ananthakrishnan R., et al. Receptor for advanced-glycation end products: key modulator of myocardial ischemic injury. Circulation 113 (2006) 1226-1234
3. Rong L.L., Gooch C., Szabolcs M., et al. RAGE: a journey from the complications of diabetes to disorders of the nervous system - striking a fine balance between injury and repair. Restor Neurol Neurosci 23 (2005) 355-365
4. Stroick M., Fatar M., Ragoschke-Schumm A., et al. Protein S-100B - a prognostic marker for cerebral damage. Curr Med Chem 13 (2006) 3053-3060
5. Zimmerman G.A., Meistrell III M., Bloom O., et al. Neurotoxicity of advanced glycation endproducts during focal stroke and neuroprotective effects of aminoguanidine. Proc Natl Acad Sci USA 92 (1995) 3744-3748
6. Cockroft K.M., Meistrell III M., Zimmerman G.A., et al. Cerebroprotective effects of aminoguanidine in a rodent model of stroke. Stroke 27 (1996) 1393-1398
7. Whitehead S., Cheng G., Hachinski V., et al. Interaction between a rat model of cerebral ischemia and beta-amyloid toxicity: II. Effects of triflusal. Stroke 36 (2005) 1782-1789
8. Whitehead S.N., Hachinski V.C., and Cechetto D.F. Interaction between a rat model of cerebral ischemia and beta-amyloid toxicity: inflammatory responses. Stroke 36 (2005) 107-112
9. Ma L., Carter R.J., Morton A.J., et al. RAGE is expressed in pyramidal cells of the hippocampus following moderate hypoxic-ischemic brain injury in rats. Brain Res 966 (2003) 167-174
10. Arancio O., Zhang H.P., Chen X., et al. RAGE potentiates A beta-induced perturbation of neuronal function in transgenic mice. Embo J 23 (2004) 4096-4105
11. Connolly Jr. E.S., Winfree C.J., Stern D.M., et al. Procedural and strain-related variables significantly affect outcome in a murine model of focal cerebral ischemia. Neurosurgery 38 (1996) 523-531 discussion 32
12. Connolly Jr. E.S., Winfree C.J., Springer T.A., et al. Cerebral protection in homozygous null ICAM-1 mice after middle cerebral artery occlusion. Role of neutrophil adhesion in the pathogenesis of stroke. J Clin Invest 97 (1996) 209-216
13. Li F., Irie K., Anwer M.S., et al. Delayed triphenyltetrazolium chloride staining remains useful for evaluating cerebral infarct volume in a rat stroke model. J Cereb Blood Flow Metab 17 (1997) 1132-1135
14. Huttunen H.J., Kuja-Panula J., Sorci G., et al. Coregulation of neurite outgrowth and cell survival by amphoterin and S100 proteins through receptor for advanced glycation end products (RAGE) activation. J Biol Chem 275 (2000) 40096-40105
15. Huttunen H.J., Fages C., and Rauvala H. Receptor for advanced glycation end products (RAGE)-mediated neurite outgrowth and activation of NF-kappaB require the cytoplasmic domain of the receptor but different downstream signaling pathways. J Biol Chem 274 (1999) 19919-19924
16. Cataldegirmen G., Zeng S., Feirt N., et al. RAGE limits regeneration after massive liver injury by coordinated suppression of TNF-alpha and NF-kappaB. J Exp Med 201 (2005) 473-484
17. Rong L.L., Yan S.F., Wendt T., et al. RAGE modulates peripheral nerve regeneration via recruitment of both inflammatory and axonal outgrowth pathways. Faseb J 18 (2004) 1818-1825