The study addressed to understand whether or not lipoproteins at low c
oncentrations could modulate Receptor-'C' dependent platelet signallin
g revealed that LDL, like exogneous cholesterol, had the capacity to i
nitiate PLD-dependent platelet signalling in a dose dependent fashion
and this effect was inhibited in presence of HDL; cAMP; DTT; Zn++ and
butanol whereas cGMP had no effect upon this PLD-dependent signalling.
Further Receptor 'C' from platelet in the purified-form displayed LDL
-or cholesterol-dependent autophosphorylation at the tyrosine residues
and this Receptor-'C' tyrosine kinase (Receptor-C-k) activity contrib
uted to the observed LDL-or cholesterol -dependent PLD activity in hum
an platelets. Based upon these results coupled with earlier results, a
n attempt was made to define the lipoprotein-dependent platelet signal
ling pathway.