RGD Reference Report - Expression and cell distribution of receptor for advanced glycation end-products in the rat cortex following experimental subarachnoid hemorrhage. - Rat Genome Database

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Expression and cell distribution of receptor for advanced glycation end-products in the rat cortex following experimental subarachnoid hemorrhage.

Authors: Li, H  Wu, W  Sun, Q  Liu, M  Li, W  Zhang, XS  Zhou, ML  Hang, CH 
Citation: Li H, etal., Brain Res. 2014 Jan 16;1543:315-23. doi: 10.1016/j.brainres.2013.11.023. Epub 2013 Nov 26.
RGD ID: 8696000
Pubmed: PMID:24291745   (View Abstract at PubMed)
DOI: DOI:10.1016/j.brainres.2013.11.023   (Journal Full-text)

Convincing evidence indicates that inflammation contributes to the adverse prognosis of subarachnoid hemorrhage (SAH). Some pro-inflammatory molecules such as high mobility group protein 1, S100 family of proteins, beta-amyloid peptide, and macrophage antigen complex 1 have been involved in the damaging inflammation process following SAH. The receptor for advanced glycation end-products (RAGE) is a transmembrane receptor that senses these molecules and plays central role in inflammatory processes. This study aimed to determine the expression and cell distribution of RAGE in the brain cortex after SAH. Male Sprague-Dawley rats were randomly divided into sham group and SAH groups at 6 h, 12 h and on day 1, day 2 and day 3 (n=6 for each subgroup). SAH groups suffered experimental SAH by injection of 0.3 ml autologous blood into the prechiasmatic cistern. RAGE expression was measured by Western blot, real-time PCR, immunohistochemistry and immunofluorescence. Nuclear expression of p65 protein, the major subunit of nuclear factor kappa B, was also detected. Our data demonstrated that the expression levels of RAGE and nuclear p65 protein were both markedly increased after SAH. Moreover, there was a significant positive correlation between the expression of RAGE and that of p65 protein. Double immunofluorescence staining showed that RAGE was expressed by neuron and microglia rather than astrocyte after SAH. These results suggest that RAGE may be directly involved in the inflammatory response after SAH, and there might be important implications for further studies using specific RAGE antagonists to decrease inflammation-mediated brain injury following SAH.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Subarachnoid Hemorrhage  ISOAger (Rattus norvegicus)8696000; 8696000mRNA and protein:increased expression:brainRGD 
Subarachnoid Hemorrhage  IEP 8696000mRNA and protein:increased expression:brainRGD 

Objects Annotated

Genes (Rattus norvegicus)
Ager  (advanced glycosylation end product-specific receptor)

Genes (Mus musculus)
Ager  (advanced glycosylation end product-specific receptor)

Genes (Homo sapiens)
AGER  (advanced glycosylation end-product specific receptor)


Additional Information