Assessment of histological features of changes in lipid metabolism in chronic hepatitis C

Jármay, K.; Karácsony, G; I, Nagy; Lonovics, János; Schaff, Z.

doi:10.1055/s-2004-826959

Cited by 9 publications

(11 citation statements)

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“…This pathway involves death receptors, such as Fas, TNF receptor, and TNF-related apoptosis-inducing ligand (TRAIL) receptors, which transduce signals to induce apoptosis upon binding to their respective ligands (52). In HCVinfected patients, the Fas-mediated signal pathway is involved in apoptosis of virus-infected hepatocytes (24). It was also reported that HCV (JFH1 strain) infection induced apoptosis through a TRAIL-mediated pathway in LH86 cells (72).…”

Section: Discussionmentioning

confidence: 99%

Hepatitis C Virus Infection Induces Apoptosis through a Bax-Triggered, Mitochondrion-Mediated, Caspase 3-Dependent Pathway

Deng

Adachi

Kitayama

et al. 2008

J Virol

149

136

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We previously reported that cells harboring the hepatitis C virus (HCV) RNA replicon as well as those expressing HCV NS3/4A exhibited increased sensitivity to suboptimal doses of apoptotic stimuli to undergo mitochondrion-mediated apoptosis (Y. Nomura-Takigawa, et al., J. Gen. Virol. 87:1935Virol. 87: -1945Virol. 87: , 2006. Little is known, however, about whether or not HCV infection induces apoptosis of the virus-infected cells. In this study, by using the chimeric J6/JFH1 strain of HCV genotype 2a, we demonstrated that HCV infection induced cell death in Huh7.5 cells. The cell death was associated with activation of caspase 3, nuclear translocation of activated caspase 3, and cleavage of DNA repair enzyme poly(ADP-ribose) polymerase, which is known to be an important substrate for activated caspase 3. These results suggest that HCV-induced cell death is, in fact, apoptosis. Moreover, HCV infection activated Bax, a proapoptotic member of the Bcl-2 family, as revealed by its conformational change and its increased accumulation on mitochondrial membranes. Concomitantly, HCV infection induced disruption of mitochondrial transmembrane potential, followed by mitochondrial swelling and release of cytochrome c from mitochondria. HCV infection also caused oxidative stress via increased production of mitochondrial superoxide. On the other hand, HCV infection did not mediate increased expression of glucose-regulated protein 78 (GRP78) or GRP94, which are known as endoplasmic reticulum (ER) stress-induced proteins; this result suggests that ER stress is not primarily involved in HCV-induced apoptosis in our experimental system. Taken together, our present results suggest that HCV infection induces apoptosis of the host cell through a Bax-triggered, mitochondrion-mediated, caspase 3-dependent pathway(s).

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Section: Discussionmentioning

confidence: 99%

Hepatitis C Virus Infection Induces Apoptosis through a Bax-Triggered, Mitochondrion-Mediated, Caspase 3-Dependent Pathway

Deng

Adachi

Kitayama

et al. 2008

J Virol

149

136

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“…Enhanced Fas-mediated hepatocyte apoptosis has been well documented in HCV-and HBV-associated chronic liver diseases; Fas expression increases in parallel with chronic hepatitis C progression, demonstrating the important role of cell death [11,23]. Infected hepatocytes exhibit enhanced Fas expression and develop increased susceptibility to FasLmediated apoptosis.…”

Section: Viral Hepatitismentioning

confidence: 99%

“…Using this method, Shimamatsu & Wanless [28] identified two types of apoptotic bodies in the liver: spherical acidophilic bodies located away from adjacent hepatocytes (Councilman bodies) and star-shaped acidophilic bodies, which are retracted but still united to hepatocytes. The apoptotic body nucleus can be pycnotic, fragmented or absent; phagocytosed apoptotic bodies, and cells exhibiting condensation of chromatin as an initial manifestation of apoptosis have also been described [21][22][23][24][25][26][27][28].…”

Section: Study Of Apoptosis Mediation In the Livermentioning

confidence: 99%

Apoptosis and progression of hepatic fibrosis in hepatitis C patients

Schinoni¹,

Paraná²,

Cavalcante³

2006

Braz J Infect Dis

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Hepatitis C is a worldwide endemic disease, affecting roughly 200 million people. It has a variable prognosis, depending on the progression to fibrosis. During the last five years, the importance of apoptosis for the pathogenesis of various diseases, including hepatitis, has been recognized. It has been suggested that an increase in T cell-apoptosis during a hepatitis C virus infection is the cause of impaired regulation of the immune cellular response, helping to maintain infection. Thus, the interest in discovering the probable mechanisms by which the hepatitis C virus perpetuates in the liver, and to determine the conditions that predispose for progression of this disease, makes investigation of apoptosis in hepatic injury of great interest. We have made an overview of the various mechanisms by which the cell, more specifically the hepatic cell, is affected by apoptosis, and how it interacts with the hepatitis C virus and the immune system.

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“…During infection with HCV, infiltrating cytotoxic T lymphocytes recognize and kill viral antigens expressed on infected hepatocytes through the Fas-Fas L pathway. However, excessive or defective Fas mediated apoptosis leads to liver failure, fibrosis, and carcinogesis (Tobi et al, 2001;Jarmay et al, 2002). Recently, Fas expression was reported to be increased in the liver of patients with chronic hepatitis C and to be directly correlated with disease activity (Anguilar et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Association of Genetic Polymorphism −670A>G in the Fas Gene and Serum Markers AST Platelet Ratio Index, AST/ALT with Significant Fibrosis and Cirrhosis in Chronic Hepatitis C

Deghady

Abdou

El-Neanaey

et al. 2012

Genetic Testing and Molecular Biomarkers

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Assessment of histological features of changes in lipid metabolism in chronic hepatitis C

Cited by 9 publications

References 0 publications

Hepatitis C Virus Infection Induces Apoptosis through a Bax-Triggered, Mitochondrion-Mediated, Caspase 3-Dependent Pathway

Hepatitis C Virus Infection Induces Apoptosis through a Bax-Triggered, Mitochondrion-Mediated, Caspase 3-Dependent Pathway

Apoptosis and progression of hepatic fibrosis in hepatitis C patients

Association of Genetic Polymorphism −670A>G in the Fas Gene and Serum Markers AST Platelet Ratio Index, AST/ALT with Significant Fibrosis and Cirrhosis in Chronic Hepatitis C

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