RGD Reference Report - Expression of HMGB1 and RAGE in rat and human brains after traumatic brain injury. - Rat Genome Database

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Expression of HMGB1 and RAGE in rat and human brains after traumatic brain injury.

Authors: Gao, TL  Yuan, XT  Yang, D  Dai, HL  Wang, WJ  Peng, X  Shao, HJ  Jin, ZF  Fu, ZJ 
Citation: Gao TL, etal., J Trauma Acute Care Surg. 2012 Mar;72(3):643-9. doi: 10.1097/TA.0b013e31823c54a6.
RGD ID: 7245557
Pubmed: PMID:22491548   (View Abstract at PubMed)
DOI: DOI:10.1097/TA.0b013e31823c54a6   (Journal Full-text)

BACKGROUND: Increasing evidence suggests that an inflammatory reaction contributes to the secondary brain injury that plays a critical role in the clinical outcome of patients with traumatic brain injury (TBI). Recently, high-mobility group box 1 (HMGB1) has been identified as a key cytokine in the inflammatory reaction and may represent a new target for the treatment of TBI. However, the expression of HMGB1 during this injury process has not yet been studied. METHODS: In this study, the levels of both HMGB1 and receptor for advanced glycation end products (RAGE) in the rat brain were analyzed by Western blot at different time points after TBI. Immunohistochemistry was also performed to examine the expression pattern of HMGB1 and RAGE in both the rat and the human brain after TBI. RESULTS: In the rat brain, HMGB1 levels significantly declined below the basal level at 6 hours after TBI and then gradually returned to the basal level 2 days later. RAGE expression increased 6 hours after TBI and reached its peak after 1 day; this level then slowly decreased but remained higher than the sham-injury group until 6 days after TBI. In both rat and human brains, HMGB1 either disappeared or was translocated from the nucleus to the cytoplasm at early stages after TBI and then was localized to the cytoplasm of phagocytic microglia at later stages. RAGE expression increased in the region surrounding the contused area after TBI in both rat and human brains. At later stages, RAGE was mainly expressed in microglia. CONCLUSION: HMGB1 is involved in both early and later stages after TBI. Targeting HMGB1 signaling may be a promising therapeutic approach for the treatment of TBI.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Brain Injuries  ISOAger (Rattus norvegicus)7245557; 7245557protein:increased expression:brain (rat)RGD 
Brain Injuries  IEP 7245557protein:increased expression:brain (rat)RGD 

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