Tags

Type your tag names separated by a space and hit enter

Molecular basis of sickle cell-endothelial cell interactions.
Curr Opin Hematol. 1996 Mar; 3(2):118-24.CO

Abstract

Adherence of sickle erythrocytes to microvascular endothelium is posited to initiate or contribute to sickle cell vaso-occlusive pain episodes. Adherence and occlusion in vivo may depend on hemodynamics interacting with plasma, erythrocyte, and endothelial cell factors. Four receptor-mediated adherence pathways have been described to date: adherence mediated by high molecular weight von Willebrand factor multimers bridging glycoprotein lb-like and integrin receptors on sickle cells and similar receptors on endothelial cells; thrombospondin bridging CD36 on sickle reticulocytes and the alpha v beta 3 integrin on large-vessel endothelial cells or alpha v beta 3 and CD36 on microvascular endothelium; binding of sickle reticulocyte alpha 4 beta 1 receptors to vascular cell adhesion molecule 1 expressed on endothelial cells stimulated by cytokine or double-stranded RNA viruses; and binding of sickle cells to endothelial cell-associated fibronectin via sickle reticulocyte alpha 4 beta 1 activated by phorbol ester or interleukin-8. The significance of these adherence pathways in sickle cell vaso-occlusion is discussed.

Authors+Show Affiliations

School of Chemical Engineering, Georgia Institute of Technology, Atlanta 30332-0100, USA.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

9372061

Citation

Wick, T M., and J R. Eckman. "Molecular Basis of Sickle Cell-endothelial Cell Interactions." Current Opinion in Hematology, vol. 3, no. 2, 1996, pp. 118-24.
Wick TM, Eckman JR. Molecular basis of sickle cell-endothelial cell interactions. Curr Opin Hematol. 1996;3(2):118-24.
Wick, T. M., & Eckman, J. R. (1996). Molecular basis of sickle cell-endothelial cell interactions. Current Opinion in Hematology, 3(2), 118-24.
Wick TM, Eckman JR. Molecular Basis of Sickle Cell-endothelial Cell Interactions. Curr Opin Hematol. 1996;3(2):118-24. PubMed PMID: 9372061.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Molecular basis of sickle cell-endothelial cell interactions. AU - Wick,T M, AU - Eckman,J R, PY - 1996/3/1/pubmed PY - 1997/12/31/medline PY - 1996/3/1/entrez SP - 118 EP - 24 JF - Current opinion in hematology JO - Curr Opin Hematol VL - 3 IS - 2 N2 - Adherence of sickle erythrocytes to microvascular endothelium is posited to initiate or contribute to sickle cell vaso-occlusive pain episodes. Adherence and occlusion in vivo may depend on hemodynamics interacting with plasma, erythrocyte, and endothelial cell factors. Four receptor-mediated adherence pathways have been described to date: adherence mediated by high molecular weight von Willebrand factor multimers bridging glycoprotein lb-like and integrin receptors on sickle cells and similar receptors on endothelial cells; thrombospondin bridging CD36 on sickle reticulocytes and the alpha v beta 3 integrin on large-vessel endothelial cells or alpha v beta 3 and CD36 on microvascular endothelium; binding of sickle reticulocyte alpha 4 beta 1 receptors to vascular cell adhesion molecule 1 expressed on endothelial cells stimulated by cytokine or double-stranded RNA viruses; and binding of sickle cells to endothelial cell-associated fibronectin via sickle reticulocyte alpha 4 beta 1 activated by phorbol ester or interleukin-8. The significance of these adherence pathways in sickle cell vaso-occlusion is discussed. SN - 1065-6251 UR - https://www.unboundmedicine.com/medline/citation/9372061/Molecular_basis_of_sickle_cell_endothelial_cell_interactions_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=9372061.ui DB - PRIME DP - Unbound Medicine ER -