In vivo regulation of inducible no synthase in immune-mediated liver injury in mice.
Standard
In vivo regulation of inducible no synthase in immune-mediated liver injury in mice. / Koerber, Kerstin; Sass, Gabriele; Kiemer, Alexandra K; Vollmar, Angelika M; Tiegs, Gisa.
In: HEPATOLOGY, Vol. 36, No. 5, 5, 2002, p. 1061-1069.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - In vivo regulation of inducible no synthase in immune-mediated liver injury in mice.
AU - Koerber, Kerstin
AU - Sass, Gabriele
AU - Kiemer, Alexandra K
AU - Vollmar, Angelika M
AU - Tiegs, Gisa
PY - 2002
Y1 - 2002
N2 - Inducible nitric oxide synthase (iNOS) has been shown to play an important role in the development of liver injury. iNOS deficiency protects mice from hemorrhage/resuscitation as well as from cytokine-mediated liver injury, for example, after administration of concanavalin A (con A). Here we investigated the in vivo effects of tumor necrosis factor (TNF)-alpha and/or interferon (IFN)-gamma, two mediators of con A-induced liver injury, the TNF receptor (TNFR) usage leading to iNOS expression, and its connection with nuclear factor kappaB (NF-kappaB) activation. In conclusion, iNOS expression in vivo is dependent on both TNF-alpha and IFN-gamma. Although con A-induced liver injury depends on both TNFR1 and TNFR2, TNF-dependent iNOS expression is mediated exclusively by TNFR1 and requires NF-kappaB activation.
AB - Inducible nitric oxide synthase (iNOS) has been shown to play an important role in the development of liver injury. iNOS deficiency protects mice from hemorrhage/resuscitation as well as from cytokine-mediated liver injury, for example, after administration of concanavalin A (con A). Here we investigated the in vivo effects of tumor necrosis factor (TNF)-alpha and/or interferon (IFN)-gamma, two mediators of con A-induced liver injury, the TNF receptor (TNFR) usage leading to iNOS expression, and its connection with nuclear factor kappaB (NF-kappaB) activation. In conclusion, iNOS expression in vivo is dependent on both TNF-alpha and IFN-gamma. Although con A-induced liver injury depends on both TNFR1 and TNFR2, TNF-dependent iNOS expression is mediated exclusively by TNFR1 and requires NF-kappaB activation.
KW - Animals
KW - Mice
KW - Mice, Inbred BALB C
KW - Mice, Inbred C57BL
KW - Mice, Knockout
KW - NF-kappa B/metabolism
KW - Concanavalin A
KW - Drug-Induced Liver Injury
KW - Nitric Oxide Synthase Type II
KW - Receptors, Tumor Necrosis Factor, Type II
KW - Signal Transduction/immunology
KW - Antibodies/pharmacology
KW - Antigens, CD/immunology/metabolism
KW - Gene Expression Regulation, Enzymologic/immunology
KW - Interferon-gamma/immunology/metabolism
KW - Liver Diseases/enzymology/immunology
KW - Nitric Oxide Synthase/genetics/immunology/metabolism
KW - Receptors, Tumor Necrosis Factor/immunology/metabolism
KW - Receptors, Tumor Necrosis Factor, Type I
KW - Tumor Necrosis Factor-alpha/immunology/metabolism
KW - Animals
KW - Mice
KW - Mice, Inbred BALB C
KW - Mice, Inbred C57BL
KW - Mice, Knockout
KW - NF-kappa B/metabolism
KW - Concanavalin A
KW - Drug-Induced Liver Injury
KW - Nitric Oxide Synthase Type II
KW - Receptors, Tumor Necrosis Factor, Type II
KW - Signal Transduction/immunology
KW - Antibodies/pharmacology
KW - Antigens, CD/immunology/metabolism
KW - Gene Expression Regulation, Enzymologic/immunology
KW - Interferon-gamma/immunology/metabolism
KW - Liver Diseases/enzymology/immunology
KW - Nitric Oxide Synthase/genetics/immunology/metabolism
KW - Receptors, Tumor Necrosis Factor/immunology/metabolism
KW - Receptors, Tumor Necrosis Factor, Type I
KW - Tumor Necrosis Factor-alpha/immunology/metabolism
M3 - SCORING: Journal article
VL - 36
SP - 1061
EP - 1069
JO - HEPATOLOGY
JF - HEPATOLOGY
SN - 0270-9139
IS - 5
M1 - 5
ER -
