LPS INDUCES SELECTIVE TRANSLOCATION OF PROTEIN-KINASE C-BETA IN LPS-RESPONSIVE MOUSE MACROPHAGES, BUT NOT IN LPS-NONRESPONSIVE MOUSE MACROPHAGES

Translocation of protein kinase C (PKC) after PMA or LPS stimulation h as been studied in thioglycolate (TGC)elicited murine peritoneal macro phages. Among the PKC subtypes we examined (alpha, beta, gamma, delta, and epsilon) by indirect immunostaining and immunoblot analysis, conv entional PKC-beta, as well as novel PKC-delta and PKC-epsilon were fou nd to exist in TGC-elicited C3H/HeN mouse macrophages. Translocation o f PKC-beta to the Triton-stable cytoskeleton could be seen in macropha ges after stimulation by both PMA and LPS. On the other hand, novel PK Cs redistributed only after PMA stimulation. Macrophages obtained from LPS-nonresponsive C3H/HeJ mice also exhibited PKC-beta, and the m.w., cellular distribution, and cellular content of this enzyme could not be distinguished from those of C3H/HeN macrophages. These macrophages exhibited PKC-delta and PKC-epsilon, as did the C3H/HeN macrophages. I n these macrophages, however, LPS did not induce any remarkable change in the intracellular distribution of PKC-delta and PKC-epsilon or PKC -beta, whereas PMA was able to induce the translocation of PKC-beta to the cytoskeleton. These results suggest that LPS stimulation induces selective redistribution of PKC-beta in LPS-responsive macrophages, wh ereas a defect related to LPS unresponsiveness exists in C3H/HeJ mouse macrophages before the PKC activation. Translocation of PKC-beta can be understood to be an important event in LPS signaling in macrophages .