• Je něco špatně v tomto záznamu ?

Sphingomyelin and phosphatidylcholine contrarily affect the induction of apoptosis in intestinal epithelial cells

K Leucht, A Fischbeck, M Caj, G Liebisch, E Hartlieb, P Benes, M Fried, HU Humpf, G Rogler, M Hausmann

. 2014 ; 58 (4) : 782-798.

Jazyk angličtina Země Německo

Perzistentní odkaz   https://www.medvik.cz/link/bmc18037787

Grantová podpora
NT13441 MZ0 CEP - Centrální evidence projektů

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.Copyright © 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc18037787
003      
CZ-PrNML
005      
20190104104309.0
007      
ta
008      
181114s2014 gw f 000 0|eng||
009      
AR
024    7_
$a 10.1002/mnfr.201300369 $2 doi
035    __
$a (PubMed)24142587
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a gw
100    1_
$a Leucht K $u Leucht, Katharina. Department of Internal Medicine, Division of Gastroenterology and Hepatology, University Hospital Zurich, Switzerland.
245    10
$a Sphingomyelin and phosphatidylcholine contrarily affect the induction of apoptosis in intestinal epithelial cells / $c K Leucht, A Fischbeck, M Caj, G Liebisch, E Hartlieb, P Benes, M Fried, HU Humpf, G Rogler, M Hausmann
520    9_
$a 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.<ovid:br /><ovid:br />Copyright &#xa9; 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
590    __
$a bohemika - dle Pubmed
650    02
$a adhezní spoje $7 D022005
650    02
$a zvířata $7 D000818
650    12
$a apoptóza $x účinky léků $7 D017209
650    02
$a protein Bid $x metabolismus $7 D051023
650    02
$a kathepsin D $x metabolismus $7 D002402
650    02
$a buněčná smrt $x účinky léků $7 D016923
650    02
$a kultivované buňky $7 D002478
650    02
$a ceramidy $x metabolismus $7 D002518
650    02
$a kolitida $x metabolismus $x patologie $7 D003092
650    02
$a potravní doplňky $7 D019587
650    12
$a epitelové buňky $x patologie $x účinky léků $7 D004847
650    02
$a ženské pohlaví $7 D005260
650    02
$a buňky HT-29 $x účinky léků $7 D019073
650    02
$a lidé $7 D006801
650    12
$a střeva $x cytologie $7 D007422
650    02
$a liposomy $x farmakologie $7 D008081
650    02
$a myši inbrední C57BL $7 D008810
650    02
$a fosfatidylcholiny $x farmakologie $x metabolismus $7 D010713
650    02
$a sfingomyelinfosfodiesterasa $x metabolismus $7 D013108
650    02
$a sfingomyeliny $x farmakologie $x metabolismus $7 D013109
700    1_
$a Fischbeck A
700    1_
$a Caj M
700    1_
$a Liebisch G
700    1_
$a Hartlieb E
700    1_
$a Beneš, Petr $7 xx0208982
700    1_
$a Fried M
700    1_
$a Humpf HU
700    1_
$a Rogler G
700    1_
$a Hausmann M
773    0_
$t Molecular Nutrition & Food Research $g Roč. 58, č. 4 (2014), s. 782-798 $p Mol Nutr Food Res $x 1613-4125 $w MED00192050
773    0_
$p Mol Nutr Food Res $g 58(4):782-98, 2014 Apr
910    __
$a ABA008 $y 4 $z 0
990    __
$a 20181114094826 $b ABA008
991    __
$a 20190104104505 $b ABA008
999    __
$a ok $b bmc $g 1350958 $s 1034817
BAS    __
$a 3
BMC    __
$a 2014 $b 58 $c 4 $d 782-798 $x MED00192050 $i 1613-4125 $m Molecular nutrition & food research
GRA    __
$a NT13441 $p MZ0
LZP    __
$a NLK 2018/lp

Najít záznam

Citační ukazatele

Možnosti archivace