RGD Reference Report - Intercellular adhesion molecule-4 and CD36 are implicated in the abnormal adhesiveness of sickle cell SAD mouse erythrocytes to endothelium. - Rat Genome Database

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Intercellular adhesion molecule-4 and CD36 are implicated in the abnormal adhesiveness of sickle cell SAD mouse erythrocytes to endothelium.

Authors: Trinh-Trang-Tan, MM  Vilela-Lamego, C  Picot, J  Wautier, MP  Cartron, JP 
Citation: Trinh-Trang-Tan MM, etal., Haematologica. 2010 May;95(5):730-7. doi: 10.3324/haematol.2009.017392. Epub 2009 Dec 16.
RGD ID: 11041114
Pubmed: PMID:20015873   (View Abstract at PubMed)
PMCID: PMC2864378   (View Article at PubMed Central)
DOI: DOI:10.3324/haematol.2009.017392   (Journal Full-text)

BACKGROUND: Abnormal adhesiveness of red blood cells to endothelium has been implicated in vaso-occlusive crisis of sickle cell disease. The present study examined whether the SAD mouse model exhibits the same abnormalities of red blood cell adhesion as those found in human sickle cell disease. DESIGN AND METHODS: The repertoire of adhesive molecules on murine erythrocytes and bEnd.3 microvascular endothelial cells was determined by flow cytometry using monoclonal antibodies or by western blotting. Adhesion was investigated in dynamic conditions and measured at different shear stresses. RESULTS: CD36, CD47 and intercellular adhesion molecular-4, but not Lutheran blood group antigen/basal cell adhesion molecule, are present on mouse mature erythrocytes. alpha(4)beta(1) are not expressed on SAD and wild type reticulocytes. Endothelial bEnd.3 cells express alpha(V)beta(3), alpha(4)beta(1), CD47, vascular cell adhesion molecule-1, and Lutheran blood group antigen/basal cell adhesion molecule, but not CD36. Adhesion of SAD red cells is: (i) 2- to 3-fold higher than that of wild type red cells; (ii) further increased on platelet activating factor-activated endothelium; (iii) not stimulated by epinephrine; (iv) inhibited after treating the endothelium with a peptide reproducing one of the binding sequences of mouse intercellular adhesion molecular-4, or with mon-oclonal antibody against murine alpha(v) integrin; and (v) inhibited after pretreatment of red blood cells with anti-mouse CD36 monoclonal antibodies. The combination of treatments with intercellular adhesion molecular-4 peptide and anti-CD36 monoclonal antibodies eliminates excess adhesion of SAD red cells. The phosphorylation state of intercellular adhesion molecular-4 and CD36 is probably not involved in the over-adhesiveness of SAD erythrocytes. CONCLUSIONS: Intercellular adhesion molecular-4/alpha(v)beta(3) and CD36/thrombospondin interactions might contribute to the abnormally high adhesiveness of SAD red cells. The SAD mouse is a valuable animal model for investigating adhesion processes of sickle cell disease.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CD36Humansickle cell anemia treatmentISOCd36 (Mus musculus) RGD 
Cd36Ratsickle cell anemia treatmentISOCd36 (Mus musculus) RGD 
Cd36Mousesickle cell anemia treatmentIMP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Cd36  (CD36 molecule)

Genes (Mus musculus)
Cd36  (CD36 molecule)

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


Additional Information