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| Description
| - Endoteliální lipotoxicita vyvolává patogenetické změny u různých stupňů kardiovaskulárních onemocnění, od časné endoteliální dysfunkce až k manifestující ateroskleróze a jejích komplikacím. Nasycené volné mastné kyseliny jsou hlavním induktorem endoteliální buněčné apoptózy a zánětlivých cytokinů. U lidí je stearoyl-CoA desaturáza-1 (hSCD-1) limitujícím enzymem katalyzujícím desaturaci nasycených kyselin na mononenasycené. Jelikož můžeme prokázat expresi SCD-1 v primárních lidských arteriálních endotelových buňkách (HAECs), pokusili jsme se dokázat kladný vliv snížené exprese hSCD-1. Na rozdíl od jiných buněk, které jsou méně citlivé na lipotoxicitu, hSCD-1 nebyla deaktivována v HAECs působením palmitátu. Na základě tohoto zjištění jsme mohli prokázat že deaktivace hSCD-1 pomocí LXR activátoru TO-901317 in HAECs chrání tyto buňky proti palmitátem indukované lipotoxicitě, buněčné apoptóze a expresi zánětlivých cytokinů IL-6 and IL-8. Zvýšena aktivita hSCD-1 byla stanovena jako poměr C16:1/16:0 a zvyšo (cs)
- Endothelial lipotoxicity has been implicated in the pathogenesis of multiple stages of cardiovascular disease from early endothelial dysfunction to manifest atherosclerosis and its complications. Saturated free fatty acids are the major inducers of endothelial cell apoptosis and inflammatory cytokines. In humans, the enzyme human stearoyl-CoA desaturase-1 (hSCD-1) is the limiting step of the desaturation of saturated to monounsaturated fatty acids. Since we could demonstrate the expression of SCD-1 in primary human arterial endothelial cells (HAECs), we aimed to prove a beneficial role of upregulated hSCD-1 expression. In contrast to other cells that are less susceptible to lipotoxicity, hSCD-1 was not upregulated in HAECs upon palmitate treatment. Following that, we could show that upregulation of hSCD-1 using the LXR activator TO-901317 in HAECs protects the cells against palmitate-induced lipotoxicity, cell apoptosis, and expression of inflammatory cytokines IL-6 and IL-8. Increased hSCD-1 activity
- Endothelial lipotoxicity has been implicated in the pathogenesis of multiple stages of cardiovascular disease from early endothelial dysfunction to manifest atherosclerosis and its complications. Saturated free fatty acids are the major inducers of endothelial cell apoptosis and inflammatory cytokines. In humans, the enzyme human stearoyl-CoA desaturase-1 (hSCD-1) is the limiting step of the desaturation of saturated to monounsaturated fatty acids. Since we could demonstrate the expression of SCD-1 in primary human arterial endothelial cells (HAECs), we aimed to prove a beneficial role of upregulated hSCD-1 expression. In contrast to other cells that are less susceptible to lipotoxicity, hSCD-1 was not upregulated in HAECs upon palmitate treatment. Following that, we could show that upregulation of hSCD-1 using the LXR activator TO-901317 in HAECs protects the cells against palmitate-induced lipotoxicity, cell apoptosis, and expression of inflammatory cytokines IL-6 and IL-8. Increased hSCD-1 activity (en)
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| Title
| - Induction of stearoyl-CoA desaturase protects human arterial endothelial cells against lipotoxicity
- Induction of stearoyl-CoA desaturase protects human arterial endothelial cells against lipotoxicity (en)
- Aktivace stearoyl-CoA desaturázy chrání lidské arteriární endotelové buňky proti lipotoxicitě (cs)
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| skos:prefLabel
| - Induction of stearoyl-CoA desaturase protects human arterial endothelial cells against lipotoxicity
- Induction of stearoyl-CoA desaturase protects human arterial endothelial cells against lipotoxicity (en)
- Aktivace stearoyl-CoA desaturázy chrání lidské arteriární endotelové buňky proti lipotoxicitě (cs)
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| skos:notation
| - RIV/00216275:25310/08:00007825!RIV09-MSM-25310___
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| http://linked.open...avai/riv/aktivita
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| http://linked.open...avai/riv/aktivity
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| http://linked.open...iv/cisloPeriodika
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| http://linked.open...vai/riv/dodaniDat
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| http://linked.open...aciTvurceVysledku
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| http://linked.open.../riv/druhVysledku
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| http://linked.open...iv/duvernostUdaju
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| http://linked.open...titaPredkladatele
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| http://linked.open...dnocenehoVysledku
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| http://linked.open...ai/riv/idVysledku
| - RIV/00216275:25310/08:00007825
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| http://linked.open...riv/jazykVysledku
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| http://linked.open.../riv/klicovaSlova
| - liver X receptor activator; inflammation; interleukin-6; interleukin-8 (en)
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| http://linked.open.../riv/klicoveSlovo
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| http://linked.open...odStatuVydavatele
| - US - Spojené státy americké
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| http://linked.open...ontrolniKodProRIV
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| http://linked.open...i/riv/nazevZdroje
| - American Journal of Physiology: Endocrinology and Metabolism
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| http://linked.open...in/vavai/riv/obor
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| http://linked.open...ichTvurcuVysledku
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| http://linked.open...cetTvurcuVysledku
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| http://linked.open...UplatneniVysledku
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| http://linked.open...v/svazekPeriodika
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| http://linked.open...iv/tvurceVysledku
| - Peter, Andreas
- Čegan, Alexander
- Staiger, Harald
- Rittig, Kilian
- Weigert, Cora
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| http://linked.open...n/vavai/riv/zamer
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| issn
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| number of pages
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| http://localhost/t...ganizacniJednotka
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| is http://linked.open...avai/riv/vysledek
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