Coagulation increases neutrophil CR1 and CR3 expression: primary role for platelet-derived growth factor.
Academic Article
Overview
abstract
Neutrophil receptors for C3b(CR1) and C3bi(CR3) mediate a number of functions important for infection control and tissue repair, such as adherence, aggregation, orientation in chemotactic gradients, and phagocytosis of opsonized particles. We studied the effect of the coagulation of whole blood on the induction of neutrophil complement receptor (CR) expression in vitro. Neutrophils incubated in serum for 1 hour at 37 degrees C increased the expression of CR1 3.43-fold and CR3 3.06-fold compared with incubation in buffer (p less than 0.001). In contrast, incubation in plasma did not induce such an increase. The serum factor responsible for this CR-inducing effect appeared to be a platelet constituent, because (1) serum derived from platelet-rich plasma, but not platelet-poor plasma, contained the CR-inducing factor; (2) pretreatment with aspirin inhibited the adenosine diphosphate-induced expression of this factor in platelet-rich plasma; (3) the CR-inducing factor was also contained in supernatants derived from frozen/thawed platelets; (4) pure platelet-derived growth factor (PDGF) induced CR expression to the same extent as did whole serum; and (5) the CR-inducing activity of serum and platelet supernatants was inhibited by incubation with antibody against PDGF but not by antibody against C5. Thus, a platelet component that is probably PDGF appears to be the major CR-inducing factor generated during in vitro coagulation and may play a vital role in mediating the neutrophil response to tissue injury and inflammation.
