Pharmacologic transglutaminase inhibition attenuates drug-primed liver hypertrophy but not Mallory body formation
A1 Originalartikel i en vetenskaplig tidskrift (referentgranskad)
Interna författare/redaktörer
Publikationens författare: Strnad P, Siegel M, Toivola DM, Choi K, Kosek JC, Khosla C, Omary MB
Förläggare: WILEY
Publiceringsår: 2006
Tidskriftsakronym: FEBS LETT
Volym: 580
Nummer: 9
Artikelns första sida, sidnummer: 2351
Artikelns sista sida, sidnummer: 2357
Antal sidor: 7
ISSN: 1873-3468
Abstrakt
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.
Nyckelord
keratin, Mallory body, transglutaminase