Inhibition of @entity715 in @entity320 allografts in XXXX by endogenous mast cell heparin.

@entity1 @entity5 @entity19 @entity54426 @entity4461 @entity715 @entity320
An unexplained paradox of @entity320 is the apparent failure of the blood within the @entity5 to clot despite the presence of multiple factors that should promote @entity4461 . Here we present histochemical evidence that @entity1 and @entity19 @entity320 are extensively infiltrated by abundant mast cells. Because mast cells contain the natural anticoagulant heparin, the present studies were aimed at defining the role of mast cell heparin in preventing the blood from clotting within B16 @entity320 grafts in C57BL/6 J @entity19 . @entity19 bearing B16 @entity320 grafts were treated with non-specific or specific inhibitors of mast cell heparin (protamine or heparinase, respectively). After the drug treatment there was histologic and functional evidence of selective @entity715 of the blood vessels within the protamine and heparinase treated @entity320 grafts. A similar, high degree of @entity715 was also observed in B16 @entity5 grown in transgenic @entity54426 knockout @entity19 bearing a targeted disruption in the gene coding for mast cell heparin synthesis. The @entity5 grown in the protamine-treated animals were significantly smaller than the @entity5 from control (untreated @entity19 ). By contrast, the @entity5 treated with heparinase or grown in the @entity54426 knockout @entity19 were significantly larger than the @entity5 from control (untreated) @entity19 . We conclude that the intrinsic procoagulant properties of @entity320 are neutralized in vivo by the anticoagulant properties of endogenous heparin produced by mast cells that naturally infiltrate the @entity5 . Our results also suggest that @entity715 and hemostasis within @entity320 may play a complex role in modulating the growth of the @entity5 .
