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c-Jun N-terminal ki...
c-Jun N-terminal kinase 2 deficiency protects against hypercholesterolemia-induced endothelial dysfunction and oxidative stress
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Osto, E. (författare)
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Matter, C. M. (författare)
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Kouroedov, A. (författare)
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Malinski, T. (författare)
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Bachschmid, M. (författare)
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Camici, G.G. (författare)
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Kilic, U. (författare)
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Stallmach, T. (författare)
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- Borén, Jan, 1963 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Wallenberglaboratoriet,Institute of Medicine, Department of Molecular and Clinical Medicine,Wallenberg Laboratory
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Iliceto, S. (författare)
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Lüscher, T.F. (författare)
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Cosentino, F. (författare)
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(creator_code:org_t)
- 2008
- 2008
- Engelska.
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Ingår i: Circulation. - 0009-7322. ; 118:20, s. 2073-80
- Relaterad länk:
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https://gup.ub.gu.se...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Background— Hypercholesterolemia-induced endothelial dysfunction due to excessive production of reactive oxygen species is a major trigger of atherogenesis. The c-Jun-N-terminal kinases (JNKs) are activated by oxidative stress and play a key role in atherogenesis and inflammation. We investigated whether JNK2 deletion protects from hypercholesterolemia-induced endothelial dysfunction and oxidative stress. Methods and Results— Male JNK2 knockout (JNK2−/−) and wild-type (WT) mice (8 weeks old) were fed either a high-cholesterol diet (HCD; 1.25% total cholesterol) or a normal diet for 14 weeks. Aortic lysates of WT mice fed a HCD showed an increase in JNK phosphorylation compared with WT mice fed a normal diet (P<0.05). Endothelium-dependent relaxations to acetylcholine were impaired in WT HCD mice (P<0.05 versus WT normal diet). In contrast, JNK2−/− HCD mice did not exhibit endothelial dysfunction (96±5% maximal relaxation in response to acetylcholine; P<0.05 versus WT HCD). Endothelium-independent relaxations were identical in all groups. A hypercholesterolemia-induced decrease in nitric oxide (NO) release of endothelial cells was found in WT but not in JNK2−/− mice. In parallel, endothelial NO synthase expression was upregulated only in JNK2−/− HCD animals, whereas the expression of antioxidant defense systems such as extracellular superoxide dismutase and manganese superoxide dismutase was decreased in WT but not in JNK2−/− HCD mice. In contrast to JNK2−/− mice, WT HCD displayed an increase in O2− and ONOO− concentrations as well as nitrotyrosine staining and peroxidation.
Nyckelord
- atherosclerosis
- endothelium
- nitric oxide
- JNK kinase
- reactive oxygen species
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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Till lärosätets databas
- Av författaren/redakt...
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Osto, E.
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Matter, C. M.
-
Kouroedov, A.
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Malinski, T.
-
Bachschmid, M.
-
Camici, G.G.
-
visa fler...
-
Kilic, U.
-
Stallmach, T.
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Borén, Jan, 1963
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Iliceto, S.
-
Lüscher, T.F.
-
Cosentino, F.
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visa färre...
- Artiklar i publikationen
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Circulation
- Av lärosätet
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Göteborgs universitet