RGD Reference Report - CD36-mediated hematoma absorption following intracerebral hemorrhage: negative regulation by TLR4 signaling. - Rat Genome Database

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CD36-mediated hematoma absorption following intracerebral hemorrhage: negative regulation by TLR4 signaling.

Authors: Fang, H  Chen, J  Lin, S  Wang, P  Wang, Y  Xiong, X  Yang, Q 
Citation: Fang H, etal., J Immunol. 2014 Jun 15;192(12):5984-92. doi: 10.4049/jimmunol.1400054. Epub 2014 May 7.
RGD ID: 11040930
Pubmed: PMID:24808360   (View Abstract at PubMed)
PMCID: PMC4049082   (View Article at PubMed Central)
DOI: DOI:10.4049/jimmunol.1400054   (Journal Full-text)

Promoting hematoma absorption is a novel therapeutic strategy for intracerebral hemorrhage (ICH); however, the mechanism of hematoma absorption is unclear. The present study explored the function and potential mechanism of CD36 in hematoma absorption using in vitro and in vivo ICH models. Hematoma absorption in CD36-deficient ICH patients was examined. Compared with patients with normal CD36 expression, CD36-deficient ICH patients had slower hematoma adsorption and aggravated neurologic deficits. CD36 expression in perihematomal tissues in wild-type mice following ICH was increased, whereas the hematoma absorption in CD36(-/-) mice was decreased. CD36(-/-) mice also showed aggravated neurologic deficits and increased TNF-alpha and IL-1beta expression levels. The phagocytic capacity of CD36(-/-) microglia for RBCs was also decreased. Additionally, the CD36 expression in the perihematoma area after ICH in TLR4(-/-) and MyD88(-/-) mice was significantly increased, and hematoma absorption was significantly promoted, which was significantly inhibited by an anti-CD36 Ab. In vitro, TNF-alpha and IL-1beta significantly inhibited the microglia expression of CD36 and reduced the microglia phagocytosis of RBCs. Finally, the TLR4 inhibitor TAK-242 upregulated CD36 expression in microglia, promoted hematoma absorption, increased catalase expression, and decreased the H2O2 content. These results suggested that CD36 mediated hematoma absorption after ICH, and TLR4 signaling inhibited CD36 expression to slow hematoma absorption. TLR4 inhibition could promote hematoma absorption and significantly improve neurologic deficits following ICH.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Hematoma treatmentISOCd36 (Mus musculus)11040930; 11040930associated with Cerebral HemorrhageRGD 
Hematoma  IEP 11040930associated with Cerebral HemorrhageRGD 
Hematoma  ISOCD36 (Homo sapiens)11040930; 11040930associated with Cerebral HemorrhageRGD 
Hematoma treatmentIEP 11040930associated with Cerebral HemorrhageRGD 

Objects Annotated

Genes (Rattus norvegicus)
Cd36  (CD36 molecule)

Genes (Mus musculus)
Cd36  (CD36 molecule)

Genes (Homo sapiens)
CD36  (CD36 molecule (CD36 blood group))

Objects referenced in this article
Gene C3 complement C3 Homo sapiens
Gene C3 complement component 3 Mus musculus
Gene C3 complement C3 Rattus norvegicus

Additional Information