PLATELET-ACTIVATING-FACTOR ACTIVATES MAPK AND INCREASES IN INTRACELLULAR CALCIUM VIA INDEPENDENT PATHWAYS IN B-LYMPHOCYTES

Platelet activating factor (PAF)-stimulation of human B-lymphoblastoid cells results in the activation of microtubule associated protein 2-k inase (MAPK) and increases in intracellular calcium. Although increase s in intracellular calcium induce MAPK activation in these cells, PAF can stimulate MAPK activation in the absence of detectable changes in intracellular calcium concentrations ([Ca2+](i)). Treatment of the LA3 50 B-lymphoblastoid cell line with either pertussis toxin (PT) or chol era toxin (CT) blocked PAF-induced changes in [Ca2+](i). However, only PT blocked PAF-induced activation of MAPK as determined by shifts in the mobility of MAPK on immunoblots. In support of this finding, only PT but not CT blocked PAF-induced phosphorylation and activation of p9 0(rsk), an event thought to be distal to MAPK activation. These result s suggest that the PAF receptor is mediating MAPK activation through p athways separate from those mediating increases in tracellular calcium . (C) 1995 Academic Press, Inc.