Sphingomyelin and phosphatidylcholine contrarily affect the induction of apoptosis in intestinal epithelial cells
| Autor: | Eva Hartlieb, Katharina Leucht, Gerhard Liebisch, Martin Hausmann, Hans-Ulrich Humpf, Anne Fischbeck, Gerhard Rogler, Petr Beneš, Michael Fried, Michaela Caj |
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| Přispěvatelé: | University of Zurich, Hausmann, Martin |
| Jazyk: | němčina |
| Rok vydání: | 2014 |
| Předmět: |
Cathepsin D
Apoptosis Pathogenesis chemistry.chemical_compound 0302 clinical medicine Cells Cultured 0303 health sciences Cell Death Adherens Junctions Colitis Sphingomyelins 3. Good health Intestines Sphingomyelin Phosphodiesterase 10219 Clinic for Gastroenterology and Hepatology Phosphatidylcholines 1305 Biotechnology Female 030211 gastroenterology & hepatology medicine.symptom Sphingomyelin HT29 Cells BH3 Interacting Domain Death Agonist Protein Biotechnology medicine.medical_specialty Ceramide Inflammation 610 Medicine & health Biology Ceramides 03 medical and health sciences Internal medicine Phosphatidylcholine medicine Animals Humans 1106 Food Science 030304 developmental biology Epithelial Cells medicine.disease Molecular biology Mice Inbred C57BL Endocrinology chemistry Dietary Supplements Liposomes Food Science |
| DOI: | 10.5167/uzh-92825 |
| Popis: | Scope The major alimentary sources for the plasma membrane lipid sphingomyelin (SM) are dairy products, eggs, and meat. We recently reported that the SM metabolite ceramide induces cathepsin D mediated apoptosis in murine intestinal epithelial cells (IECs) and increases inflammation in acute colitis. We investigated the impact of SM and phosphatidylcholine on apoptosis in human IECs and point out BH3-interacting death agonist (BID) as link between cathepsin D and apoptosis. Methods and results HT-29 and isolated human IECs were stimulated with SM or phosphatidylcholine. SM treatment resulted in increased apoptosis. Phosphatidylcholine showed contrary effects. Western revealed higher amounts of cathepsin D and BID activation upon lipid stimulation. Western blotting revealed BID activation through SM in both an induced and a spontaneous mouse model of colitis. Conclusion Dietary phospholipids may induce or abolish apoptosis in IECs and seem to play a role in the pathogenesis of inflammatory bowel diseases. This nutritional factor might be considered when evaluating the pathogenesis of inflammatory bowel diseases. Effects of SMase- and SM treatment on inflammation in dextran sulfate sodium induced animal models of colitis and in vitro experiments are discussed as controversial. Variable sources of SM, feeding techniques, and mouse strains might play a role. |
| Databáze: | OpenAIRE |
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