Accessibility navigation


Renal cells activate the platelet receptor CLEC-2 through podoplanin.

Christou, C. M., Pearce, A. C., Watson, A. A., Mistry, A. R., Pollitt, A. Y., Fenton-May, A. E., Johnson, L. A., Jackson, D. G., Watson, S. P. and O'Callaghan, C. A. (2008) Renal cells activate the platelet receptor CLEC-2 through podoplanin. The Biochemical journal, 411 (1). pp. 133-40. ISSN 1470-8728

[img] Text
· Restricted to Repository staff only
· The Copyright of this document has not been checked yet. This may affect its availability.

2MB

It is advisable to refer to the publisher's version if you intend to cite from this work. See Guidance on citing.

Abstract/Summary

We have recently shown that the C-type lectin-like receptor, CLEC-2, is expressed on platelets and that it mediates powerful platelet aggregation by the snake venom toxin rhodocytin. In addition, we have provided indirect evidence for an endogenous ligand for CLEC-2 in renal cells expressing HIV-1. This putative ligand facilitates transmission of HIV through its incorporation into the viral envelope and binding to CLEC-2 on platelets. The aim of the present study was to identify the ligand on these cells which binds to CLEC-2 on platelets. Recombinant CLEC-2 exhibits specific binding to HEK-293T (human embryonic kidney) cells in which the HIV can be grown. Furthermore, HEK-293T cells activate both platelets and CLEC-2-transfected DT-40 B-cells. The transmembrane protein podoplanin was identified on HEK-293T cells and was demonstrated to mediate both binding of HEK-293T cells to CLEC-2 and HEK-293T cell activation of CLEC-2-transfected DT-40 B-cells. Podoplanin is expressed on renal cells (podocytes). Furthermore, a direct interaction between CLEC-2 and podoplanin was confirmed using surface plasmon resonance and was shown to be independent of glycosylation of CLEC-2. The interaction has an affinity of 24.5+/-3.7 microM. The present study identifies podoplanin as a ligand for CLEC-2 on renal cells.

Item Type:Article
Refereed:Yes
Divisions:Life Sciences > School of Biological Sciences > Biomedical Sciences
ID Code:44805

University Staff: Request a correction | Centaur Editors: Update this record

Page navigation