Pharmacologic transglutaminase inhibition attenuates drug-primed liver hypertrophy but not Mallory body formation

A1 Journal article (refereed)


Internal Authors/Editors


Publication Details

List of Authors: Strnad P, Siegel M, Toivola DM, Choi K, Kosek JC, Khosla C, Omary MB
Publisher: WILEY
Publication year: 2006
Journal acronym: FEBS LETT
Volume number: 580
Issue number: 9
Start page: 2351
End page: 2357
Number of pages: 7
ISSN: 1873-3468


Abstract

Mallory bodies (MBs) are characteristic of several liver disorders, and consist primarily of keratins with transglutaminase-generated keratin crosslinks. We tested the effect of the transglutaminase-2 (TG2) inhibitor KCC009 on MB formation in a mouse model fed 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC). KCC009 decreased DDC-induced liver enlargement without affecting NIB formation or extent of liver injury. TG2 protein and activity increased after DDC feeding and localized within and outside hepatocytes. KCC009 inhibited DDC-induced hepatomegaly by affecting hepatocyte cell size rather than proliferation. Hence, TG2 is a potential mediator of injury-induced hepatomegaly via modulation of hepatocyte hypertrophy, and KCC009-mediated TG2 inhibition does not affect mouse MB formation. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.


Keywords

keratin, Mallory body, transglutaminase

Last updated on 2019-21-10 at 01:36