Effects of protein kinase inhibitors on the stimulated neutrophil responses by degraded immunoglobulin G.
Effects of protein kinase C inhibitors, staurosporine and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine dihydrochloride and protein tyrosine kinase inhibitors, genistein, tyrphostin and 2,5-dimethylcinnamate on the neutrophil responses stimulated by immunoglobulin G (IgG), complement C5a or platelet-activating factor were studied. After receptor binding, the role of protein kinase C and protein tyrosine kinase in the stimulation of neutrophil responses, superoxide production and lysosomal enzyme release in degraded IgG-activated neutrophils may be similar to chemoattractant-stimulated cells. In contrast to complement C5a or platelet-activating factor, protein tyrosine kinase appears to play an important role in the regulation of intracellular Ca2+ mobilization in neutrophils activated by degraded IgG rather than by protein kinase C.
Ahn
S K
SK
Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, South Korea.
Shin
Y K
YK
Kang
H J
HJ
Han
E S
ES
Lee
C S
CS
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002417:Cattle; D019833:Genistein; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism*; D007529:Isoflavones / Q000494:pharmacology; D008247:Lysosomes / Q000201:enzymology; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism; D011493:Protein Kinase C / Q000037:antagonists & inhibitors* / Q000502:physiology; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors* / Q000502:physiology; D016897:Respiratory Burst / Q000187:drug effects* / Q000502:physiology; D019311:Staurosporine / Q000494:pharmacology; D013481:Superoxides / Q000378:metabolism
D007074:Immunoglobulin G; D007529:Isoflavones; D013481:Superoxides; D019833:Genistein; D011505:Protein-Tyrosine Kinases; D011493:Protein Kinase C; D019311:Staurosporine; D002118:Calcium