In:
FEBS Letters, Wiley, Vol. 516, No. 1-3 ( 2002-04-10), p. 63-66
Kurzfassung:
Heme oxygenase‐1 (HO‐1) is induced under various oxidative stress conditions, such as lipopolysaccharide (LPS) insult. Induction of HO‐1 by LPS is reported to be mediated through interleukin‐1β (IL‐1β), rather than other inflammatory cytokines in the mouse liver. However, we found that IL‐1α/β knockout (KO) mice responded well to LPS insult, as did wild‐type mice with respect to HO‐1 mRNA induction (about 30‐fold increase). In contrast, tumor necrosis factor α KO (TNFαKO) mice responded very weakly to LPS in the HO‐1 mRNA expression, but not metallothionein mRNA. Recent studies reveal that nitric oxide from Kupffer cells is involved in HO‐1 induction in the liver produced by LPS. Therefore, nitrite and nitrate concentrations in the liver were also measured and these parameters did not increase in either IL‐1KO or TNFαKO. In addition, the phosphorylation of c‐JUN N‐terminal kinase (JNK) and p38, but not extracellular signal‐regulated kinase, was very low in TNFαKO mice due to LPS administration. All of these findings indicate that TNFα is a major candidate to trigger HO‐1 induction in response to LPS stimulation, and that its message is likely transduced through JNK and p38 pathways.
Materialart:
Online-Ressource
ISSN:
0014-5793
,
1873-3468
DOI:
10.1016/S0014-5793(02)02502-4
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2002
ZDB Id:
1460391-3
SSG:
12
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