Glycine blocks opening of a death channel in cultured hepatic sinusoidal endothelial cells during chemical hypoxia
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چکیده
منابع مشابه
In hepatic fibrosis, liver sinusoidal endothelial cells acquire enhanced immunogenicity.
The normal liver is characterized by immunologic tolerance. Primary mediators of hepatic immune tolerance are liver sinusoidal endothelial cells (LSECs). LSECs block adaptive immunogenic responses to Ag and induce the generation of T regulatory cells. Hepatic fibrosis is characterized by both intense intrahepatic inflammation and altered hepatic immunity. We postulated that, in liver fibrosis, ...
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The hepatic sinusoids are lined by a unique population of hepatic sinusoidal endothelial cells (HSEC), which is one of the first hepatic cell populations to come into contact with blood components. However, HSEC are not simply barrier cells that restrict the access of bloodborne compounds to the parenchyma. They are functionally specialised endothelial cells that have complex roles, including n...
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We assessed the effects of dexamethasone on hypoxia-induced dysfunction of the pulmonary endothelium using organ-cultured rabbit intrapulmonary arteries. Three μM dexamethasone inhibited the 7 day-hypoxia (5% oxygen)-induced impairments of endothelial dependent relaxation, cGMP accumulation, and increase in intracellular Ca level under substance P-stimulated conditions. Treatment with dexametha...
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Insulin signaling in vascular endothelial cells (ECs) is critical to maintain endothelial function but also to mediate insulin action on peripheral glucose disposal. However, gene knockout studies have reached disparate conclusions. Thus, insulin receptor inactivation in ECs does not impair insulin action, whereas inactivation of Irs2 does. Previously, we have shown that endothelial ablation of...
متن کاملDexamethasone blocks hypoxia-induced endothelial dysfunction in organ-cultured pulmonary arteries.
We assessed the effects of dexamethasone (DEX) on hypoxia-induced dysfunction of the pulmonary endothelium using organ-cultured rabbit intrapulmonary arteries; 3-microM DEX inhibited the 7-day hypoxia (5% oxygen)-induced impairments of endothelial-dependent relaxation, cGMP accumulation, and increase in intracellular Ca(2+) level under substance P-stimulated conditions. Treatment with DEX over ...
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ژورنال
عنوان ژورنال: Cell Death & Differentiation
سال: 2001
ISSN: 1350-9047,1476-5403
DOI: 10.1038/sj.cdd.4400877