Transplanted hepatocytes engraft, survive, and proliferate in the liver of rats with carbon tetrachloride-induced cirrhosis

Singh, Gaurav; Rajvanshi, Pankaj; Sokhi, Rana P.; Slehria, Sanjeev; Palestro, Christopher J.; Bhargava, Kuldeep K.; Gupta, Sanjeev

doi:10.1002/(sici)1096-9896(200005)191:1<78::aid-path587>3.0.co;2-p

Cited by 57 publications

(25 citation statements)

References 28 publications

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“…31,32 Continuous exposure to this toxin produces progressive liver injury and fibrosis, eventually causing cirrhosis, portal hypertension and death. 33,34 The main cause of acute liver injury by CCl 4 is free radicals of its metabolites. Activation of CCl 4 by liver cytochrome P-450 generates methyltrichloride radicals (CCl 3 ).…”

Section: Discussionmentioning

confidence: 99%

MRI-based texture analysis: a potential technique to assess protectors against induced-liver fibrosis in rats

Mahmoud‐Ghoneim¹,

Amin²,

Corr³

2009

Radiology and Oncology

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Section: Discussionmentioning

confidence: 99%

MRI-based texture analysis: a potential technique to assess protectors against induced-liver fibrosis in rats

Mahmoud‐Ghoneim¹,

Amin²,

Corr³

2009

Radiology and Oncology

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“…This process is followed by the release of inflammatory mediators from activated hepatic macrophages, which are believed to potentiate the CCl 4 -induced hepatic injury. Discrete exposure to CCl 4 results in acute liver injury; continuous exposure to this toxin produces progressive liver injury and fibrosis, eventually causing cirrhosis, portal hypertension, and death (2).…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of a Mixture of Aloe vera and Silybum marianum Against Carbon Tetrachloride–Induced Acute Hepatotoxicity and Liver Fibrosis

et al. 2009

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Abstract. The hepatoprotective effects of ACTIValoe ® N-931 complex, a mixture of Aloe vera and Silybum marianum, against acute and chronic carbon tetrachloride (CCl 4 )-induced liver injuries were investigated. Acute hepatotoxicity was induced by intraperitoneal injection of CCl 4 (50 μl / kg), and ACTIValoe ® N-931 complex at 85, 170, and 340 mg / kg was administered orally 48, 24, and 2 h before and 6 h after injection of CCl 4 . Hepatotoxicity was assessed 24 h after CCl 4 treatment. Liver fibrosis was induced by intraperitoneal injection of CCl 4 for 8 weeks (0.5 ml / kg, twice per week), and mice were treated with ACTIValoe ® N-931 complex at 85, 170, or 340 mg / kg once a day (p.o.). In both acute hepatotoxicity and liver fibrosis, serum aminotransferase levels and lipid peroxidation were increased and the hepatic glutathione content was decreased. These changes were prevented by ACTIValoe

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“…We took advantage of the interesting characteristics of the AX16, HBx-expressing, transgenic line (16,52), that expresses a moderate amount of HBx soon after birth, the levels declining as the animals become older. Furthermore, we benefited from recent advances in liver cell transplantation, which may offer new experimental approaches to address these issues (53)(54)(55). We reasoned that the transplantation of HBx-expressing hepatocytes isolated from HBx-expressing transgenic mice into nontransgenic mouse liver, and the induction of liver regeneration by partial hepatectomy would indeed allow us to investigate the effects of HBx expression in the context of a low percentage of HBx-expressing liver cells undergoing in vivo proliferation.…”

mentioning

confidence: 99%

Paracrine in vivo inhibitory effects of hepatitis B virus X protein (HBx) on liver cell proliferation: An alternative mechanism of HBx-related pathogenesis

Tralhão

Roudier

Morosan

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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The role of the hepatitis B virus X protein (HBx) in the pathogenesis of hepatitis B virus (HBV) infection remains unclear. HBx exhibits pleiotropic biological effects, whose in vivo relevance is a matter for debate. In the present report, we have used a combination of HBx-expressing transgenic mice and liver cell transplantation to investigate the in vivo impact of HBx expression on liver cell proliferation and viability in a regenerative context. We show that moderate HBx expression inhibits liver regeneration after partial hepatectomy in HBx-expressing transgenic mice. We also demonstrate that the transplantation of HBx-expressing liver cells, isolated from HBx transgenic mice, is sufficient to inhibit overall recipient liver regeneration after partial hepatectomy. Moreover, the injection of serum samples drawn from HBx-expressing transgenic mice mimicked the inhibitory effect of HBx on liver regeneration. Finally, the incubation of primary rat hepatocytes with the supernatant of HBx-expressing liver cells inhibits cellular DNA synthesis. Taken together, our results demonstrate a paracrine inhibitory effect of HBx on liver cell proliferation and lead us to propose HBV as one of the few viruses implicated in human cancer which act, at least in part, through paracrine biological pathways.

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Transplanted hepatocytes engraft, survive, and proliferate in the liver of rats with carbon tetrachloride-induced cirrhosis

Cited by 57 publications

References 28 publications

MRI-based texture analysis: a potential technique to assess protectors against induced-liver fibrosis in rats

MRI-based texture analysis: a potential technique to assess protectors against induced-liver fibrosis in rats

Protective Effect of a Mixture of Aloe vera and Silybum marianum Against Carbon Tetrachloride–Induced Acute Hepatotoxicity and Liver Fibrosis

Paracrine in vivo inhibitory effects of hepatitis B virus X protein (HBx) on liver cell proliferation: An alternative mechanism of HBx-related pathogenesis

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