RGD Reference Report - Complement C3 participates in the function and mechanism of traumatic brain injury at simulated high altitude. - Rat Genome Database

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Complement C3 participates in the function and mechanism of traumatic brain injury at simulated high altitude.

Authors: Wei, Linjie  Zhang, Jianbo  Zhang, Bo  Geng, Junjun  Tan, Qiang  Wang, Ling  Chen, Zhi  Feng, Hua  Zhu, Gang 
Citation: Wei L, etal., Brain Res. 2020 Jan 1;1726:146423. doi: 10.1016/j.brainres.2019.146423. Epub 2019 Oct 22.
RGD ID: 408418727
Pubmed: PMID:31654641   (View Abstract at PubMed)
DOI: DOI:10.1016/j.brainres.2019.146423   (Journal Full-text)


BACKGROUND: Traumatic brain injury (TBI) leads to severe mortality and disability, in which secondary injury induced by complement activation plays an important role. TBI tends to be associated with more severe cerebral edema and worse neurological functional recovery if it occurs in high-altitude areas than in low-altitude areas. However, the underlying mechanism of this difference is unknown. Thus, we used cobra venom factor (CVF) to deplete complement C3 in simulated high-altitude areas to explore whether the differences in outcome at different altitudes are related to secondary injury caused by complement C3.
METHODS: The weight-drop model was adopted to induce TBI in rats. Rats were randomly divided into the following groups: sham + saline (sham), high altitude + TBI + saline (HAT), high altitude + TBI + CVF (H-CVF), low altitude + TBI + saline (LAT), and low altitude + TBI + CVF (L-CVF). Brain contusion and edema volumes, brain water content, myelin basic protein (MBP) expression, tumor necrosis factor alpha (TNF-a) expression, interleukin 1 beta (IL1B) expression, mortality rate, neurological function, and complement component 3 (C3) mRNA expression were measured by techniques such as Evans blue fluorescence, Perls staining, TUNEL staining, ELISA, immunohistochemistry and Western blotting to evaluate correlations between complement activation and secondary injury.
RESULTS: The activation of complement after TBI was significantly higher at high altitude than at low altitude. High-altitude TBI resulted in a leakier blood-brain barrier, more severe cerebral edema and higher mortality than low-altitude TBI did. In addition, high-altitude TBI tended to be associated with more MBP degradation, ferric iron deposition, neuronal apoptosis, and inflammatory factor deposition than low-altitude TBI. All of these effects of TBI were partially reversed by inhibiting complement activation using CVF.
CONCLUSION: Our study provided evidence that TBI at high altitude leads to severe edema and high mortality and disability rates. Complement C3 activation is one of the important factors contributing to secondary brain injury.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
C3RatBrain Contusion amelioratesIMP  RGD 
C3HumanBrain Contusion amelioratesISOC3 (Rattus norvegicus) RGD 
C3MouseBrain Contusion amelioratesISOC3 (Rattus norvegicus) RGD 
IL1BHumanBrain Contusion treatmentISOIl1b (Rattus norvegicus) RGD 
Il1bRatBrain Contusion treatmentIEP  RGD 
Il1bMouseBrain Contusion treatmentISOIl1b (Rattus norvegicus) RGD 
TNFHumanBrain Contusion treatmentISOTnf (Rattus norvegicus) RGD 
TnfRatBrain Contusion treatmentIEP  RGD 
TnfMouseBrain Contusion treatmentISOTnf (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
C3  (complement C3)
Il1b  (interleukin 1 beta)
Tnf  (tumor necrosis factor)

Genes (Mus musculus)
C3  (complement component 3)
Il1b  (interleukin 1 beta)
Tnf  (tumor necrosis factor)

Genes (Homo sapiens)
C3  (complement C3)
IL1B  (interleukin 1 beta)
TNF  (tumor necrosis factor)


Additional Information