https://transhumanist.ru/index.php?action=history&feed=atom&title=ACSL5 2026-09-06T18:30:08Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=ACSL5&diff=4239&oldid=prev 2021-04-29T19:07:53Z

<p>Новая страница: «Long-chain-fatty-acid--CoA ligase 5 (EC 6.2.1.3) (Arachidonate--CoA ligase) (EC 6.2.1.15) (Long-chain acyl-CoA synthetase 5) (LACS 5) [ACS5] [FACL5] [UNQ633/PRO12...»</p> <p><b>Новая страница</b></p><div>Long-chain-fatty-acid--CoA ligase 5 (EC 6.2.1.3) (Arachidonate--CoA ligase) (EC 6.2.1.15) (Long-chain acyl-CoA synthetase 5) (LACS 5) [ACS5] [FACL5] [UNQ633/PRO1250]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Ageing sensitized by iPLA β deficiency induces liver fibrosis and intestinal atrophy involving suppression of homeostatic genes and alteration of intestinal lipids and bile acids.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28888832<br /> |abstract=Ageing is a major risk factor for various forms of liver and gastrointestinal (GI) disease and genetic background may contribute to the pathogenesis of these diseases. Group VIA phospholipase A2 or iPLA β is a homeostatic PLA by playing a role in phospholipid metabolism and remodeling. Global iPLA β mice exhibit aged-dependent phenotypes with body weight loss and abnormalities in the bone and brain. We have previously reported the abnormalities in these mutant mice showing susceptibility for chemical-induced liver injury and colitis. We hypothesize that iPLA β deficiency may sensitize with ageing for an induction of GI injury. Male wild-type and iPLA β mice at 4 and 20-22months of age were studied. Aged, but not young, iPLA β mice showed increased hepatic fibrosis and biliary ductular expansion as well as severe intestinal atrophy associated with increased apoptosis, pro-inflammation, disrupted tight junction, and reduced number of mucin-containing globlet cells. This damage was associated with decreased expression of intestinal endoplasmic stress [[XBP1]] and its regulator HNF1α, FATP4, [[ACSL5]], bile-acid transport genes as well as nuclear receptors LXRα and FXR. By LC/MS-MS profiling, iPLA β deficiency in aged mice caused an increase of intestinal arachidonate-containing phospholipids concomitant with a decrease in ceramides. By the suppression of intestinal FXR/FGF-15 signaling, hepatic bile-acid synthesis gene expression was increased leading to an elevation of secondary and hydrophobic bile acids in liver, bile, and intestine. In conclusions, ageing sensitized by iPLA β deficiency caused a decline of key intestinal homeostatic genes resulting in the development of GI disease in a gut-to-liver manner.<br /> |mesh-terms=* Aging<br /> * Animals<br /> * Bile Acids and Salts<br /> * Ceramides<br /> * Group VI Phospholipases A2<br /> * Intestinal Diseases<br /> * Liver Cirrhosis<br /> * Mice<br /> * Mice, Knockout<br /> * Phospholipids<br /> |keywords=* Ageing<br /> * FXR<br /> * Intestinal homeostasis<br /> * Lipidomics<br /> * Pla2G6<br /> * XBP1<br /> |full-text-url=https://sci-hub.do/10.1016/j.bbalip.2017.09.001<br /> }}</div>

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