Role of extracellular and intracellular nitric oxide in the regulation of macrophage responses.
We studied the role of nitric oxide in the stress response and apoptosis. Intracellular nitric oxide potentiated the stress response. However, intracellular nitric oxide suppressed the stress response in macrophages of proinflammatory and antiinflammatory phenotypes. Intracellular nitric oxide promoted apoptosis in macrophages of the proinflammatory phenotype, but inhibited this process in cells of the antiinflammatory phenotype. Exogenous nitric oxide synthesized by macrophages protected them from lipopolysaccharide-induced apoptosis. Our results indicate that nitric oxide produces various effects on the stress response and apoptosis in macrophages, which depends on modus operandi.
Malysheva
E V
EV
Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow.
Kruglov
S V
SV
Khomenko
I P
IP
Bakhtina
L Yu
LY
Pshennikova
M G
MG
Manukhina
E B
EB
Malyshev
I Yu
IY
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D017209:Apoptosis; D002478:Cells, Cultured; D053938:DNA Fragmentation; D007249:Inflammation; D008070:Lipopolysaccharides / Q000378:metabolism; D008262:Macrophage Activation; D008264:Macrophages / Q000378:metabolism*; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism*; D010641:Phenotype
D000893:Anti-Inflammatory Agents; D008070:Lipopolysaccharides; D009569:Nitric Oxide