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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 03375naa a2200433 4500 | |
| 001 | oai:gup.ub.gu.se/85813 | |
| 003 | SwePub | |
| 008 | 240528s2008 | |||||||||||000 ||eng| | |
| 024 | 7 | a https://gup.ub.gu.se/publication/858132 URI |
| 024 | 7 | a https://doi.org/10.1161/CIRCULATIONAHA.108.7650322 DOI |
| 040 | a (SwePub)gu | |
| 041 | a eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Osto, E.4 aut |
| 245 | 1 0 | a c-Jun N-terminal kinase 2 deficiency protects against hypercholesterolemia-induced endothelial dysfunction and oxidative stress |
| 264 | 1 | c 2008 |
| 520 | a 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. | |
| 653 | a atherosclerosis | |
| 653 | a endothelium | |
| 653 | a nitric oxide | |
| 653 | a JNK kinase | |
| 653 | a reactive oxygen species | |
| 700 | 1 | a Matter, C. M.4 aut |
| 700 | 1 | a Kouroedov, A.4 aut |
| 700 | 1 | a Malinski, T.4 aut |
| 700 | 1 | a Bachschmid, M.4 aut |
| 700 | 1 | a Camici, G.G.4 aut |
| 700 | 1 | a Kilic, U.4 aut |
| 700 | 1 | a Stallmach, T.4 aut |
| 700 | 1 | a Borén, Jan,d 1963u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Wallenberglaboratoriet,Institute of Medicine, Department of Molecular and Clinical Medicine,Wallenberg Laboratory4 aut0 (Swepub:gu)xborej |
| 700 | 1 | a Iliceto, S.4 aut |
| 700 | 1 | a Lüscher, T.F.4 aut |
| 700 | 1 | a Cosentino, F.4 aut |
| 710 | 2 | a Göteborgs universitetb Institutionen för medicin, avdelningen för molekylär och klinisk medicin4 org |
| 773 | 0 | t Circulationg 118:20, s. 2073-80q 118:20<2073-80x 0009-7322 |
| 856 | 4 8 | u https://gup.ub.gu.se/publication/85813 |
| 856 | 4 8 | u https://doi.org/10.1161/CIRCULATIONAHA.108.765032 |
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- Kilic, U.
- Stallmach, T.
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