Cre-estrogen receptor-mediated hepatitis C virus structural protein expression in mice

Tumurbaatar, Batbayar; Sun, Yixiao; Chan, Teh Sheng; Sun, Jiaren

doi:10.1016/j.jviromet.2007.05.025

Cited by 14 publications

(13 citation statements)

References 48 publications

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“…Despite overwhelming evidence from in vivo (transgenic and humanized mice) and in vitro studies to indicate that HCV infection causes ER stress and induces the UPR, we still need to confirm the presence of ER stress in hepatitis C patients by conducting clinical studies at single cells level (Liberman et al, 1999;Tardif et al, 2002Tardif et al, , 2004Benali-Furet et al, 2005;Egan, 2005, 2009;Ciccaglione et al, 2005Ciccaglione et al, , 2007Zheng et al, 2005;Tumurbaatar et al, 2007;Sekine-Osajima et al, 2008;Joyce et al, 2009;Li et al, 2009;Mishima et al, 2010;Von Dem Bussche et al, 2010;Funaoka et al, 2011;Merquiol et al, 2011;Shinohara et al, 2013). Clinical data will need to be further corroborated and elaborated using well-controlled experiments.…”

Section: Discussionmentioning

confidence: 99%

Unfolded protein response in hepatitis C virus infection

Chan

2014

Front. Microbiol.

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Hepatitis C virus (HCV) is a single-stranded, positive-sense RNA virus of clinical importance. The virus establishes a chronic infection and can progress from chronic hepatitis, steatosis to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The mechanisms of viral persistence and pathogenesis are poorly understood. Recently the unfolded protein response (UPR), a cellular homeostatic response to endoplasmic reticulum (ER) stress, has emerged to be a major contributing factor in many human diseases. It is also evident that viruses interact with the host UPR in many different ways and the outcome could be pro-viral, anti-viral or pathogenic, depending on the particular type of infection. Here we present evidence for the elicitation of chronic ER stress in HCV infection. We analyze the UPR signaling pathways involved in HCV infection, the various levels of UPR regulation by different viral proteins and finally, we propose several mechanisms by which the virus provokes the UPR.

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Section: Discussionmentioning

confidence: 99%

Unfolded protein response in hepatitis C virus infection

Chan

2014

Front. Microbiol.

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“…The activated Cre-ER translocates to the nucleus and mediates DNA recombination between the loxP sequences present in the transgene. This system has been used to obtain sustained expression of HCV structural proteins in the liver 63 in double-transgenic mice that express CRE-ER as well as an albumin promoter-driven transgene construct containing the core, E1, and E2-p7 sequences of genotype HCV 1b, carrying a spacer containing stop codons in all three reading frames, and flanked by loxP sequences at both ends (Fig. 6).…”

Section: Cre-mediated Gene Expression or Disruptionmentioning

confidence: 99%

Mouse Models of Hepatocellular Carcinoma

Fausto

Campbell

2010

Semin Liver Dis

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The etiology of liver cancer is well known, but despite recent progress in the application of molecular techniques for the analysis of the development of these tumors, we still lack precise knowledge about pathogenesis of hepatocellular carcinoma (HCC). Animal models can provide essential knowledge about HCC pathogenesis, particularly if they mimic the tissue environment in which human tumors develop. The synergism between studies in animal models and human tumors is strengthened by using comparative genomic analysis to identify genes and pathways that are critical for both mouse and human oncogenesis. In this article, the authors discuss some selective examples of constitutive, conditional, and inducible models of HCC development, and briefly describe the genetic manipulations required for engineering these models and some new techniques used for gene screening in HCC. The authors focus on models that best correlate with the human disease and offer important insights into the pathogenesis of HCC.

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“…examples of temporal correlations include time courses of reovirus and WNV infection, which show that apoptosis occurs concurrently with, or slightly after, the appearance of viral antigen16,26. In addition, in the livers of transgenic mice that express HBV and HCV proteins, the expression or recognition of viral antigen triggers apoptosis27,28.…”

Section: Viruses Induce Apoptosis In Vivomentioning

confidence: 99%

“…Colocalization of apoptosis and virus antigen in individual cells can also be detected in the CNS following infection with Theiler’s murine encephalomyelitis virus (TMeV)32, SINV33 and reovirus34,35, in the hearts of CVB3-infected mice19 and in the livers of transgenic mice that express HCV and HBV proteins28,36.…”

Section: Viruses Induce Apoptosis In Vivomentioning

confidence: 99%

“…In addition, in vivo evidence supporting direct viral induction of apoptosis has come from models in which apoptotic injury occurs in the absence of, or prior to, an obvious immune response. For example, apoptosis occurs following infection of the CNS and heart with reovirus16,21,30, and shortly after the induction of protein expression in transgenic mice that conditionally express HCV structural proteins in the liver28 in the presence of little, or no, infiltrating immune cells. This shows that immune cells are not required for apoptosis in these models.…”

Section: The Immune System In Virus-induced Apoptosismentioning

confidence: 99%

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Apoptosis in animal models of virus-induced disease

2009

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Apoptosis is associated with virus-induced human diseases of the central nervous system, heart and liver, and causes substantial morbidity and mortality. Although virus-induced apoptosis is well characterized in individual cells in cell culture, virus-induced apoptosis in vivo and the role of apoptosis in virus-induced disease is not well established. This Review focuses on animal models of virus-induced diseases of the central nervous system, heart and liver that provide insights into the role of apoptosis in pathogenesis, the pathways involved and the potential therapeutic implications.Apoptosis plays an essential part in homeostasis, development and human disease by facilitating the removal of unwanted, damaged or infected cells. However, apoptosis may also have a pathogenic role by contributing to cell death and tissue injury. Apoptotic cell death occurs in a wide range of human viral infections, including infections of the central nervous system (CNS), heart and liver. For example, apoptosis can be detected in the brains of patients with virus-induced CNS disease, including patients with HIV-1-associated dementia 1 , herpes simplex virus (HSV) 2,3 and cytomegalovirus (CMV) 3 encephalitis. Furthermore, apoptotic cells can be observed in the diseased human heart during both active and chronic viral myocarditis 4 , and hepatocyte apoptosis is emerging as an important feature of liver injury in patients with hepatitis B virus (HBV) and hepatitis C virus (HCV) infections [5][6][7][8][9][10] .The morphological and nuclear changes associated with apoptosis are typically caused by the sequential activation of a family of aspartate-specific cysteine proteases called caspases [11][12][13] (BOX 1). Caspase 3, the main executioner caspase, can be activated by the initiator caspase, caspase 8, following activation of cell-surface death receptors in the extrinsic apoptotic pathway (BOX 1 ; FIG. 1). Alternatively, the intrinsic apoptotic pathway can activate caspase 3 following release of pro-apoptotic factors from the mitochondria and activation of the initiator caspase, caspase 9 (BOX 1 ; FIG. 1). In some cell types (type I cells), activation of caspase 8 is sufficient for apoptosis. However, in other cell types (type II cells), apoptosis requires intrinsic apoptotic signalling, which can be activated directly or through extrinsic apoptotic signalling through the caspase 8-dependent cleavage of BCL-2 interacting domain death agonist (BID), a member of the BH3-only B-cell lymphoma protein 2 family (BOX 2 ; FIG. Correspondence to P.C. Penny.Clarke@uchsc.edu. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript 1). Caspase 3 can also be activated by granzyme B, a serine protease found in cytotoxic T lymphocytes (CTLs) (FIG. 1). Granzyme B can also cleave BID, forming the truncated protein gtBID and resulting in the activation of intrinsic apoptotic signalling 14 . Granzyme B and extrinsic apoptotic signalling constitute the two major components of CTL-induced cell death. B...

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Cre-estrogen receptor-mediated hepatitis C virus structural protein expression in mice

Cited by 14 publications

References 48 publications

Unfolded protein response in hepatitis C virus infection

Unfolded protein response in hepatitis C virus infection

Mouse Models of Hepatocellular Carcinoma

Apoptosis in animal models of virus-induced disease

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