CLEC-2-dependent activation of mouse platelets is weakly inhibited by cAMP but not by cGMP.

ABSTRACT:

Background

The activation of platelet CLEC-2 by podoplanin on lymphatic endothelial cells (LECs) has a critical role in prevention of mixing of lymphatic and blood vasculatures during embryonic development. Paradoxically, LECs release cAMP and cGMP-elevating agents, prostacyclin (PGI2 ) and nitric oxide (NO), respectively, which are powerful inhibitors of platelet activation. This raises the question of how podoplanin is able to activate CLEC-2 in the presence of the inhibitory cyclic nucleotides.

Objectives

We investigated the influence of cyclic nucleotides on CLEC-2 signaling in platelets.

Methods

We used rhodocytin, CLEC-2 monoclonal antibody, LECs and recombinant podoplanin as CLEC-2 agonists on mouse platelets. The effects of the cyclic nucleotide-elevating agen

SUBMITTER: Borgognone A 

PROVIDER: S-EPMC4138994 | biostudies-literature | 2014 Apr

REPOSITORIES: biostudies-literature