RAGE mediates vascular injury and inflammation after global cerebral ischemia

Kamide, Tomoya; Kitao, Yasuko; Takeichi, Toshiaki; Okada, Akiko; Mohri, Hiromi; Schmidt, Ann Marie; Kawano, Takayuki; Munesue, Seiichi; Yamamoto, Yasuhiko; Yamamoto, Hiroshi; Hamada, Jun-ichiro; Hori, Osamu

doi:10.1016/j.neuint.2011.12.008

Cited by 56 publications

(75 citation statements)

References 28 publications

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“…10,29 In addition, RAGE is involved in inflammation and edema after traumatic brain injury and ischemia. 11,30 Consistent with these reports, we found that FPS-ZM1 administration suppressed RAGE and NF-κB p65 expression and brain edema, and improved motor function 24 hours after ICH. The inhibition of RAGE expression by FPS-ZM1 was likely because of a positive-feedback mechanism because RAGE activated by Aβ promotes the generation of reactive oxygen species and NF-κB activation, and increases the expression of RAGE itself.…”

Section: Discussionsupporting

confidence: 88%

Receptor for Advanced Glycation End-Product Antagonist Reduces Blood–Brain Barrier Damage After Intracerebral Hemorrhage

Yang

Wang

Zhang³

et al. 2015

Stroke

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Background and Purpose-To determine whether the receptor for advanced glycation end-products (RAGE) plays a role in early brain injury from intracerebral hemorrhage (ICH), RAGE expression and activation after injury were examined in a rat model of ICH with or without administration of a RAGE-specific antagonist (FPS-ZM1). Methods-Autologous arterial blood was injected into the basal ganglia of rats to induce ICH. The motor function of the rats was examined, and water content was detected after euthanization. Blood-brain barrier permeability was determined by Evans blue staining and colloidal gold nanoparticle tracers. Nerve fiber injury in white matter was determined by diffusion tensor imaging analysis, and the expression of target genes was analyzed by Western blotting and quantitative reverse transcription polymerase chain reaction. FPS-ZM1 was administered by intraperitoneal injection. Results-Expression of RAGE and its ligand high-mobility group protein B1 were increased at 12 hours after ICH, along with blood-brain barrier permeability and perihematomal nerve fiber injury. RAGE and nuclear factor-κB p65 upregulation were also observed when FeCl 2 was infused into the basal ganglia at 24 hours. FPS-ZM1 administration resulted in significant improvements of blood-brain barrier damage, brain edema, motor dysfunction, and nerve fiber injury, and the expression of RAGE, nuclear factor-κB p65, proinflammatory mediators interleukin 1β, interleukin-6, interleukin-8R, cyclooxygenase-2, inducible nitric oxide synthase, and matrix metallopeptidase-9 was attenuated. Moreover, decreases in claudin-5 and occludin expression were partially recovered. FPS-ZM1 also reversed FeCl 2 -induced RAGE and nuclear factor-κB p65 upregulation. Conclusions-RAGE signaling is involved in blood-brain barrier and white matter fiber damage after ICH, the initiation of which is associated with iron. RAGE antagonists represent a novel therapeutic intervention to prevent early brain injury after ICH. .).The online-only Data Supplement is available with this article at http://stroke.ahajournals.org/lookup/suppl

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Section: Discussionsupporting

confidence: 88%

Receptor for Advanced Glycation End-Product Antagonist Reduces Blood–Brain Barrier Damage After Intracerebral Hemorrhage

Yang

Wang

Zhang³

et al. 2015

Stroke

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“…This phenomenon is probably related to movement of soluble A␤ peptide from blood into brain tissue [54,55]. Finally, it was noted that RAGE mediated additionally delayed neuronal death by enhancing vascular wall injury and neuroinflammation [56].…”

Section: Discussionmentioning

confidence: 97%

Discrepancy in Expression of β-Secretase and Amyloid-β Protein Precursor in Alzheimer-Related Genes in the Rat Medial Temporal Lobe Cortex Following Transient Global Brain Ischemia

Pluta

Kocki

Ułamek-Kozioł³

et al. 2016

JAD

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Abstract. Brain ischemia may be causally related with Alzheimer's disease. Presumably, ␤-secretase and amyloid-␤ protein precursor gene expression changes may be associated with Alzheimer's disease neuropathology. Consequently, we have examined quantitative changes in both ␤-secretase and amyloid-␤ protein precursor genes in the medial temporal lobe cortex with the use of quantitative rtPCR analysis following 10-min global brain ischemia in rats with survival of 2, 7, and 30 days. The greatest significant overexpression of ␤-secretase gene was noted on the 2nd day, while on days 7-30 the expression of this gene was only modestly downregulated. Amyloid-␤ protein precursor gene was downregulated on the 2nd day, but on days 7-30 postischemia, there was a significant reverse tendency. Thus, the demonstrated alterations indicate that the considerable changes of expression of ␤-secretase and amyloid-␤ protein precursor genes may be connected with a response of neurons in medial temporal lobe cortex to transient global brain ischemia. Finally, the ischemia-induced gene changes may play a key role in a late and slow onset of Alzheimer-type pathology.

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“…A receptor has been identified for AGEs in tissue and called RAGE (Neeper et al, 1992;Schmidt et al, 1992). This protein RAGE is expressed in a variety of cell types involved in the complications from diabetes including endothelial cells but has also been localized to neurons and microglia in the CNS (Kamide et al, 2012;Muhammad et al, 2008). RAGE is a multiligand member of the immunoglobulin superfamily and has been shown to bind other molecules in addition to AGEs including amphoterin (also known as high mobility group box 1 (HMGB1)) S100 proteins, amyloid beta and recently the macrophage cell surface antigen MAC-1 (Chavakis et al, 2003;Hofmann et al, 1999;Hori et al, 1995;Schmidt et al, 1996).…”

Section: A Role For Rage?mentioning

confidence: 99%

Ischemia-induced hyperglycemia: Consequences, neuroendocrine regulation, and a role for RAGE

Weil

2012

Hormones and Behavior

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RAGE mediates vascular injury and inflammation after global cerebral ischemia

Cited by 56 publications

References 28 publications

Receptor for Advanced Glycation End-Product Antagonist Reduces Blood–Brain Barrier Damage After Intracerebral Hemorrhage

Receptor for Advanced Glycation End-Product Antagonist Reduces Blood–Brain Barrier Damage After Intracerebral Hemorrhage

Discrepancy in Expression of β-Secretase and Amyloid-β Protein Precursor in Alzheimer-Related Genes in the Rat Medial Temporal Lobe Cortex Following Transient Global Brain Ischemia

Ischemia-induced hyperglycemia: Consequences, neuroendocrine regulation, and a role for RAGE

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