TY - JOUR
T1 - Lipopolysaccharide enhances interferon-γ-induced nitric oxide (NO) production in murine vascular endothelial cells via augmentation of interferon regulatory factor-1 activation
AU - Koide, Naoki
AU - Mya Mya., Mu
AU - Hassan, Ferdaus
AU - Islam, Shamima
AU - Tumurkhuu, Gantsetseg
AU - Dagvadorj, Jargalsaikhan
AU - Naiki, Yoshikazu
AU - Mori, Isamu
AU - Yoshida, Tomoaki
AU - Yokochi, Takashi
PY - 2007/6
Y1 - 2007/6
N2 - Lipopolysaccharide (LPS) enhances the production of nitric oxide (NO) in interferon (IFN)-γstimulated vascular endothelial cells. We studied the mechanism by which LPS enhances IFN-γ-induced NO production by using the murine vascular endothelial cell line, END-D. LPS enhanced IFN-γinduced NO production via augmented expression of inducible type NO synthase (iNOS) mRNA. LPS significantly augmented the activation of interferon regulatory factor (IRF)-1 in IFN-γ-stimulated END-D cells, although it did not affect the activation of either MyD88-dependent nuclear factor (NF)-κB or MyD88-independent IRF-3. SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK), prevented the nuclear translocation of IRF-1 in LPS and IFN-γ-stimulated END-D cells, and inhibited the iNOS expression and NO production in those cells. Therefore, it is proposed that LPS enhanced NO production in IFN-γ-stimulated END-D cells via augmenting p38 MAPKmediated IRF-1 activation.
AB - Lipopolysaccharide (LPS) enhances the production of nitric oxide (NO) in interferon (IFN)-γstimulated vascular endothelial cells. We studied the mechanism by which LPS enhances IFN-γ-induced NO production by using the murine vascular endothelial cell line, END-D. LPS enhanced IFN-γinduced NO production via augmented expression of inducible type NO synthase (iNOS) mRNA. LPS significantly augmented the activation of interferon regulatory factor (IRF)-1 in IFN-γ-stimulated END-D cells, although it did not affect the activation of either MyD88-dependent nuclear factor (NF)-κB or MyD88-independent IRF-3. SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK), prevented the nuclear translocation of IRF-1 in LPS and IFN-γ-stimulated END-D cells, and inhibited the iNOS expression and NO production in those cells. Therefore, it is proposed that LPS enhanced NO production in IFN-γ-stimulated END-D cells via augmenting p38 MAPKmediated IRF-1 activation.
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U2 - 10.1177/0968051907080894
DO - 10.1177/0968051907080894
M3 - Article
C2 - 17621559
AN - SCOPUS:34548446002
SN - 0968-0519
VL - 13
SP - 167
EP - 175
JO - Journal of Endotoxin Research
JF - Journal of Endotoxin Research
IS - 3
ER -
