2013
DOI: 10.1002/hep.26335
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Interstrain differences in chronic hepatitis and tumor development in a murine model of inflammation-mediated hepatocarcinogenesis

Abstract: Chronic inflammation is strongly associated with an increased risk for hepatocellular carcinoma (HCC) development. The multidrug resistance 2 (Mdr2)-knockout (KO) mouse (adenosine triphosphate-binding cassette b4 2/2 ), a model of inflammation-mediated HCC, develops chronic cholestatic hepatitis at an early age and HCC at an adult age. To delineate factors contributing to hepatocarcinogenesis, we compared the severity of early chronic hepatitis and late HCC development in two Mdr2-KO strains: Friend virus B-ty… Show more

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Cited by 36 publications
(32 citation statements)
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“…Gene expression was evaluated either by semi-qRT-PCR [15], or by real-time RT-PCR as described in the Supplementary Methods using primers described in Supplementary Table 1. Total liver protein was isolated and analyzed by immunoblotting as previously described [15]. …”
Section: Methodsmentioning
confidence: 99%
See 1 more Smart Citation
“…Gene expression was evaluated either by semi-qRT-PCR [15], or by real-time RT-PCR as described in the Supplementary Methods using primers described in Supplementary Table 1. Total liver protein was isolated and analyzed by immunoblotting as previously described [15]. …”
Section: Methodsmentioning
confidence: 99%
“…Interestingly, Gal1 acts by promoting HCC cell adhesion through PI3K and/or ERK1/2 signaling pathways [14]. In murine HCC models, we have demonstrated that an inefficient anti-inflammatory activity of the endogenous Gal1 is associated with increased inflammation at an early age and with enhanced tumor development at an older age [15]. On the other hand, the tumor-promoting effect of the hepatitis C virus (HCV) transgene in the chronic inflammation-mediated HCC mouse model, was associated with increased Gal1 expression in the liver [16].…”
Section: Introductionmentioning
confidence: 99%
“…Wild-type B6 mice were obtained from Envigo RMS Ltd. (Jerusalem, Israel); the Lgals1-KO mutants of the B6 strain were kindly provided by Prof. Francoise Poirier (Institut Jacques Monod, Universités P6 and P7, Paris, France) and propagated in our facility. The Mdr2-KO/B6 and Gal1-KO/FVB mice were generated in our laboratory (21,22). The dKO/FVB and dKO/B6 strains we generated by mating Gal1-KO with Mdr2-KO mice of either B6 or FVB backgrounds to generate F1 double heterozygous mice.…”
Section: Micementioning
confidence: 99%
“…Thus, Gal1 may have a dual effect on tumor development mediated by chronic inflammation, acting either as an inhibitory mediator at the early inflammatory stage of a disease or protumorigenic at the later stages. Importantly, we have previously demonstrated that loss of Gal1 differentially affects response of the FVB/NJ (FVB) and C57BL/6 (B6) inbred mouse strains to acute liver inflammation (21). In order to reveal the role of Gal1 in HCC development, we generated double mutants Mdr2-KO/Lgals1-KO on the FVB and B6 genetic backgrounds and compared HCC development in these strains with their parental Mdr2-KO strains for both sexes.…”
mentioning
confidence: 99%
“…However, the severity of cholestatic liver damage, induced by loss of Mdr2, depends on the genetic background of mice. 10 The authors compared the efficiency of liver regeneration and HCC development in Mdr2 −/− and double-deficient Mdr2 −/− p21 Waf1/Cip1−/− mice in the C57BL/6 genetic background which displayed moderate liver injury. They demonstrate that p21 Waf1/Cip1 acts oncogenically in this model since its loss significantly delayed liver tumour incidence in aged Mdr2 −/− p21 Waf1/Cip1−/− mice.…”
mentioning
confidence: 99%