Effect of prolactin on nitric oxide and interleukin-1 production of murine peritoneal macrophages: role of Ca2+ and protein kinase C.
In vitro treatment of macrophages with prolactin (PRL) was found to increase the production of nitric oxide (NO) and interleukin-1 (IL-1). Production of NO and IL-1 by macrophages got additively enhanced on simultaneous treatment with LPS and PRL. The production of NO was, however, decreased when the macrophages were treated with a combination of PRL and nifedipine, a Ca2+ blocker indicating a role of Ca2+ in the activation of macrophages with PRL. PRL-treated macrophages showed an enhanced translocation of protein kinase C (PKC) from cytosol to the membrane, indicating that PRL activates macrophages via the activation of PKC.
Kumar
A
A
Department of Zoology, University of Delhi, India.
Singh
S M
SM
Sodhi
A
A
D000818:Animals; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002478:Cells, Cultured; D005260:Female; D007375:Interleukin-1 / Q000096:biosynthesis*; D017737:Macrophages, Peritoneal / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009543:Nifedipine / Q000494:pharmacology; D009569:Nitric Oxide / Q000096:biosynthesis*; D011388:Prolactin / Q000494:pharmacology*; D011493:Protein Kinase C / Q000502:physiology*; D013047:Specific Pathogen-Free Organisms
D002121:Calcium Channel Blockers; D007375:Interleukin-1; D009569:Nitric Oxide; D011388:Prolactin; D011493:Protein Kinase C; D009543:Nifedipine; D002118:Calcium