Knock-Out of beta-Glucosidase 2 Has No Influence on Dextran Sulfate Sodium-Induced Colitis

Scharl, Michael and Leucht, Katharina and Frey-Wagner, Isabelle and Zeitz, Jonas and Hausmann, Martin and Fischbeck, Anne and Liebisch, Gerhard and Kellermeier, Silvia and Pesch, Theresa and Arikkat, Joba and Schmitz, Gerd and Fried, Michael and Yildiz, Yildiz and Rogler, Gerhard (2011) Knock-Out of beta-Glucosidase 2 Has No Influence on Dextran Sulfate Sodium-Induced Colitis. DIGESTION, 84 (2). pp. 156-167. ISSN 0012-2823,

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Abstract

Background/Aims: The non-lysosomal glucosylceramidase, beta-glucosidase (Gba2), hydrolyzes glucosylceramide to glucose and ceramide (Cer). Cer is a potent second-messenger lipid that plays an important role in signaling cascades involved in apoptosis. The aim of this study was to investigate whether Gba2 knock-out (Gba2(-/-)) affects the extent of dextran sulfate sodium (DSS)-induced colitis in mice. Methods: Acute colitis was induced in wild-type (WT) and Gba2(-/-) mice by administration of 2% DSS in drinking water. After 7 days, mice underwent colonoscopy and were sacrificed. Results: Both DSS-treated WT (n = 10) and Gba2(-/-) (n = 12) mice showed elevated histological and endoscopic scores compared to respective H(2)O controls (n = 9 each). However, no

Item Type: Article
Uncontrolled Keywords: NITRIC-OXIDE; MICE; APOPTOSIS; CERAMIDE; BETA-GLUCOSIDASE-2; REGENERATION; PURIFICATION; COLONOSCOPY; DISEASE; DEATH; beta-Glucosidase; DSS colitis; Ceramide; Apoptosis; Cell regeneration
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Klinische Chemie und Laboratoriumsmedizin
Depositing User: Dr. Gernot Deinzer
Date Deposited: 29 Jun 2020 10:33
Last Modified: 29 Jun 2020 10:33
URI: https://pred.uni-regensburg.de/id/eprint/21557

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