Paracrine up-regulation of monocyte cyclooxygenase-2 by platelets: Role of transforming growth factor-β1

摘要: Objective : To examine the role of platelets and platelet-derived products on cyclooxygenase-2 (Cox-2) induction in adherent monocytes to address signaling pathways involved. Methods Platelets were obtained from peripheral blood healthy donors. Adherent co-cultured with autologous or platelet releasates exposed mediators contained α-granules (either source recombinant) for 4–24 h. Cox-2 protein mRNA determined by Western RT-PCR analysis, respectively. Thromboxane B2 (TxB2) prostaglandin E2 (PGE2) synthesis as index activity, levels transforming growth factor-β1 (TGF-β1) measured enzyme immunoassay (EIA). Results Activated induce rapid transient de novo monocytes. The effect is dependent upon number but not cell–cell contact. Platelet-induced was affected prevention TxA2 microparticle formation blunted inhibition α-granule secretion. TGF-β1, either recombinant (rTGF-β1), induced expression activity at concentrations within range those detected activated platelets; this shared factor (rPDGFBB). time course TGF-β1 identical that observed releasates. Moreover, receptor blockade completely abolished platelet-induced expression. p38 MAPK activation represents a common transduction pathway through which rTGF-β1 monocytes. Conclusion These findings suggest released has pivotal further supports key inflammatory reparative responses.