The Effects of Serum from Patients with Acute Liver Failure on the Growth and Metabolism of Hep G2 Cells

Shi, Qingde; Gaylor, J.D.S.; Cousins, Roderick; Plevris, John; Hayes, Peter; Grant, M.H.

doi:10.1046/j.1525-1594.1998.06211.x

Cited by 29 publications

(16 citation statements)

References 25 publications

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“…As liver tumor cells, C3A cells can be obtained through isolation from human liver tumor tissues and cloning. They perform the basic functions of normal hepatocytes without a carcinogenic effect, and have therefore been widely used in clinical and experimental research of the in vitro liver support system (Shi et al, 1998;Liu et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Establishment of cytochrome P450 3A4 and glutathione S-transferase A1-transfected human hepatoma cell line and functional analysis

Chang¹,

You²,

Liu³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. This study aimed to enhance the drug metabolism function of the human hepatoma cell line C3A and to explore the related significance for patients with severe liver disease. The important liver phase I and phase II drug metabolism enzymes, cytochrome P450 3A4 (CYP 3A4) and glutathione S-transferase A1 (GST A1), were constructed into a double expression vector and then transfected into C3A cells. Furthermore, in order to increase the expression of CYP 3A4 and GST A1, they were optimized according to human optimal codons. Another double-expression vector, pBudCE4.1-optimized CYP 3A4-optimized GST A1, was constructed and then transfected into C3A to establish a stable cell line. The drug metabolism function of C3A was evaluated. Sequence determination and analysis results showed that the recombinant plasmid pBudCE4.1-CYP 3A4-GST A1 met the application standard and its transfection was successful. The expression and activity of CYP 3A4 and GST A1 in unoptimized C3A cells were higher than those in blank C3A cells. Unoptimized C3A had a better drug metabolism function. Although some C3A cells transfected with pBudCE4.1-optimized CYP 3A4-optimized GST A1 survived, they grew slowly, and were therefore not applicable in clinical practice. Unoptimized C3A is superior to blank C3A in drug metabolism, and could be applied in the bioartificial liver support system as a new material.

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Section: Discussionmentioning

confidence: 99%

Establishment of cytochrome P450 3A4 and glutathione S-transferase A1-transfected human hepatoma cell line and functional analysis

Chang¹,

You²,

Liu³

et al. 2014

Genet. Mol. Res.

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“…Indeed, it has already been shown that incubating liver cells with serum from patients with fulminant hepatic failure (FHF serum) for as little as 4 h decreased protein, RNA and DNA synthesis, as well as ion transport, cell integrity and cell adhesion [19,20].…”

Section: Introductionmentioning

confidence: 99%

Improvement of C3A cell metabolism for usage in bioartificial liver support systems

Filippi

Keatch

Rangar

et al. 2004

Journal of Hepatology

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“…17 A clear understanding does not exist of which factors in liver injury modulate the engraftment and survival of transplanted cells. Serum from patients with FHF has been shown to induce a dose-dependent inhibition of proliferation 18 -24 and protein synthesis, 25 and in some studies induces cell death. 23,26,27 Is there a change in the hepatic microenvironment, making it less receptive to engraftment, or is there a change in the hepatocyte phenotype so that it is less likely to engraft?…”

mentioning

confidence: 99%

Serum from patients with fulminant hepatic failure causes hepatocyte detachment and apoptosis by a β1-integrin pathway

et al. 2004

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Hepatocyte transplantation is restricted by the impaired ability of hepatocytes to engraft and survive in the damaged liver. Understanding the mechanisms that control this process will permit the development of strategies to improve engraftment. We studied changes in liver matrix during acute injury and delineated the mechanisms that perturb the successful adhesion and engraftment of hepatocytes. Collagen IV expression was increased in sinusoidal endothelium and portal tracts of fulminant hepatic failure explants, whereas there were minimal changes in the expression of fibronectin, tenascin, and laminin. Using an in vitro model of cellular adhesion, hepatocytes were cultured on collagen-coated plates and exposed to serum from patients with liver injury to ascertain their subsequent adhesion and survival. There was a rapid, temporally progressive decrease in the adhesive properties of hepatocytes exposed to such serum that occurred within 4 hours of exposure. Loss of activity of the ␤1-integrin receptor, which controls adhesion to collagen, was seen to precede this loss of adhesive ability. Addition of the ␤1-integrin activating antibody (TS2/16) to cells cultured with liver injury serum significantly increased their adhesion to collagen, and prevented significant apoptosis. In conclusion, we have identified an important mechanism that underpins the failure of infused hepatocytes to engraft and survive in liver injury. Pretreating cells with an activating antibody can improve their engraftment and survival, indicating that serum from patients with liver injury exerts a defined nontoxic biological effect. This finding has important implications in the future of cellular transplantation for liver and other organ diseases. (HEPATOLOGY 2004;40:636 -645.)

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The Effects of Serum from Patients with Acute Liver Failure on the Growth and Metabolism of Hep G2 Cells

Cited by 29 publications

References 25 publications

Establishment of cytochrome P450 3A4 and glutathione S-transferase A1-transfected human hepatoma cell line and functional analysis

Establishment of cytochrome P450 3A4 and glutathione S-transferase A1-transfected human hepatoma cell line and functional analysis

Improvement of C3A cell metabolism for usage in bioartificial liver support systems

Serum from patients with fulminant hepatic failure causes hepatocyte detachment and apoptosis by a β1-integrin pathway

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