NDLI: Intracellular and extracellular NO differentially modulates the stress response and apoptosis in macrophages exposed to the influence of biological or physical factors

Content Provider	Springer Nature Link
Author	Malysheva, E. V. Kruglov, S. V. Nazarov, V. A. Manukhina, E. B. Malyshev, I. Yu.
Copyright Year	2007
Abstract	We studied the role of extracellular and intracellular NO in the regulation of the stress response and apoptosis in macrophages of proinflammatory and antiinflammatory phenotypes under the influence of S. aureus and heat shock. Blockade of extracellular nitric oxide synthesis in cells with antiinflammatory phenotype inhibited the stress response induced by S. aureus and heat shock. The decrease in extracellular nitric oxide concentration around antiinflammatory macrophages potentiated the stress response induced by S. aureus, but had no effect on the stress response induced by heat shock. Hence, intracellular NO mediates the stress response induced by S. aureus and heat shock, while extracellular NO inhibits the stress response induced by S. aureus, but has no effect on the stress response induced by heat shock. In cells with antiinflammatory phenotype, intracellular NO plays an antiapoptotic role. S. aureus and heat shock did not cause apoptosis in macrophages with proinflammatory phenotype, while intracellular NO did not play a role in antiapoptotic activity of the proinflammatory phenotype. Extracellular NO synthesized by macrophages protects these cells from apoptosis induced by S. aureus and heat shock.
Starting Page	673
Ending Page	677
Page Count	5
File Format	PDF
ISSN	00074888
Journal	Bulletin of Experimental Biology and Medicine
Volume Number	143
Issue Number	6
e-ISSN	15738221
Language	English
Publisher	Springer US
Publisher Date	2007-01-01
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	stress response apoptosis macrophages nitric oxide Biomedicine general Internal Medicine Cell Biology Pathology Laboratory Medicine
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry, Genetics and Molecular Biology

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