Function of bcl-X proteins in Nitric Oxide-induced Apoptosis in RAW 264.7 Macrophages / 대한면역학회지
Korean Journal of Immunology
;
: 229-236, 1999.
Article
Dans Coréen
| WPRIM
| ID: wpr-224757
ABSTRACT
LPS and IFN-r induce nitric oxide synthase in macrophages and the resultant NO causes apoptotic cell death in the activated macrophages. NO production and apoptosis were inhibited by N-monomethyl L-arginine (NMMA), a competitive inhibitor of NO synthase. To study the role of BCL-X proteins, RAW 264.7 cells were transfected with the expression vectors with human bcl-Xl or bcl-Xs cDNAs, respectively. Stable transfectants were selected and confirmed by RT-PCR. NO production in response to LPS and IFN-r caused apoptosis in RAW 264.7 cells and vector transfected control cells within 24 hr. Both NO production and apoptosis were inhibited by N(G)-monomethyl L-arginine (NMMA). In contrast, bcl-Xs transfectant appeared slightly susceptible and bcl-X(L)< transfectant appeared slightly resistant, although NO production was similar to control cells. These results suggest that bcl-X proteins play roles in both positive and negative regulation of apoptosis induced by NO.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Arginine
/
Mort cellulaire
/
Apoptose
/
ADN complémentaire
/
Nitric oxide synthase
/
Protéine bcl-X
/
Macrophages
/
Monoxyde d'azote
Limites du sujet:
Humains
langue:
Coréen
Texte intégral:
Korean Journal of Immunology
Année:
1999
Type:
Article
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