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Tsamandas, Athanassios C.; Thomopoulos, Konstantinos; Gogos, Charalambos; Tepetes, Konstantinos; Kourelis, Theodore; Ravazoula, Panagiota; Petsas, Theodore; Bonikos, Dionysis S.; Karatza, Chrisoula; Karavias, Dionissios

doi:10.1023/a:1015839807627

Cited by 11 publications

(2 citation statements)

References 14 publications

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“…Bcl-2 expression was localized in bile ducts and mononuclear cells in CHC, but was not commonly present in hepatocytes (31). In CHC with cirrhosis, Bcl-2 expression was also found in bile ducts and mononuclear cells, but in contrast to CHC without cirrhosis, Bcl-2 was also expressed in hepatocytes.…”

Section: Discussionmentioning

confidence: 99%

Significance of increased expression of decoy receptor 3 in chronic liver disease

Kim¹,

Kotoula

Hytiroglou

et al. 2009

Digestive and Liver Disease

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Background/Aims Considerable evidence has indicated that apoptosis plays an important role in hepatocyte death in chronic liver disease. However, the cellular and molecular mechanisms underlying liver regeneration in the disease are largely unknown. Plausibly, certain molecules expressed to counteract apoptosis might provide survival advantage of certain liver cells. Therefore, we investigated a possible expression of decoy receptor 3 (DcR3) of the tumor necrosis factor (TNF) receptor family in chronic liver diseases since DcR3 is known to inhibit apoptosis mediated by pro-apoptotic TNF family ligands including FasL. Methods A series of liver biopsies from patients with different stages of fibrosis were subjected to immunohistochemistry and in situ hybridization. Results Both DcR3 protein and mRNA were mainly expressed in biliary epithelial cells and infiltrating lymphocytes in the diseased livers. Most noticeably, intense DcR3 expression was observed in newly developing biliary ductules in regenerative nodules as well as dysplastic nodules of cirrhotic livers. In addition, DcR3 secretion in hepatocellular carcinoma (HCC) cells in culture was via the activation of mitogen-activated protein kinases. Conclusion DcR3 was specifically expressed in chronic liver diseases and HCC cells, and DcR3 might facilitate the survival of liver cells by exerting its anti-apoptotic activity during the progression of liver cirrhosis and hepatocarcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Significance of increased expression of decoy receptor 3 in chronic liver disease

Kim¹,

Kotoula

Hytiroglou

et al. 2009

Digestive and Liver Disease

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“… 15 In patients with acute and chronic hepatitis (CH), the expression of apoptosis-related proteins was shown to be linked with intrahepatic bile-duct development. 16 The change in 25-hydroxyvitamin D (25[OH]D) levels in the serum of patients with CH is significantly associated with the expression of apoptosis-related proteins, especially in HCC subjects. 17 …”

Section: Introductionmentioning

confidence: 99%

Correlation between vitamin D levels and apoptosis in geriatric patients infected with hepatitis C virus genotype 4

Gabr¹,

Alghadir²,

Allam³

et al. 2016

CIA

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BackgroundVitamin D levels play a pivotal role in most biological processes and differ according to age. A deficiency of vitamin D in chronic hepatitis C (CHC) patients has been shown to be linked with the severity of liver fibrosis, but little is known about the mechanism of this association.ObjectiveIn this study, we evaluate the potential interrelation between vitamin D levels, oxidative stress, and apoptosis, based on liver fibrosis in geriatric patients infected with hepatitis C virus (HCV) genotype 4.Subjects and methodsA total of 120 adult individuals aged 30–68 years were recruited in this study. Of these, 20 healthy subjects (15 men and five women) with a mean age of 48.3±6.1 years were selected as controls, and 100 patients with a mean age of 47.8±4.9 years with chronic HCV (CHC) who had undergone liver biopsy (80 men and 20 women) were included in this study. Based on liver radiographic (computed tomography, magnetic resonance imaging) and histological Metavir system analyses, the CHC patients were classified into three groups: asymptomatic CHC carriers (n=30), fibrosis (n=25), and cirrhosis (n=45). HCV RNA, HCV genotypes, inflammatory cytokines AFP and TNFα, 25-hydroxyvitamin D (25[OH]D) levels, apoptotic markers single-stranded DNA (ssDNA) and soluble Fas (sFas), and oxidative stress markers nitric oxide (NO) and total antioxidant capacity (TAC) were estimated by using molecular, immunoassay, and colorimetric techniques.ResultsApproximately 30% of the study population (n=30) were diagnosed as asymptomatic CHC carriers, and 70% of the study population (n=70) had severe fibrosis; these were classified into fibrosis and cirrhosis. There was a significant reduction in 25(OH)D levels and TAC activity, along with an increase in levels of NO, AFP, TNFα, ssDNA, and sFas in fibrosis and cirrhosis subjects compared with those of asymptomatic CHC carriers and health controls. The deficiency in 25(OH)D levels correlated positively with sFas, ssDNA, AFP, TNFα, NO, and TAC, and negatively with age, sex, liver function, body mass index, homeostatic model assessment – insulin resistance, HCV RNA, and viral load. Significant intercorrelation was reported between serum 25(OH)D concentrations and apoptotic and oxidative markers, which suggested progression of liver pathogenesis and fibrogenesis via oxidative and apoptotic mechanisms.ConclusionThe data showed that vitamin D status was significantly correlated with pathogenesis and fibrogenesis of the liver in geriatric patients infected with HCV genotype 4. The deficiency in 25(OH)D levels was shown to have a pivotal role in the pathogenesis of liver via apoptotic, oxidative stress, and inflammatory mechanistic pathways. The data point to adequate vitamin D levels being recommended for a good response to treatment strategies, especially in older CHC patients.

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HCV-Associated B Cell Clonalities in the Liver Do Not Carry the t(14;18) Chromosomal Translocation *

Sansonno

Tucci

et al. 2005

Hepatology

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H epatitis C virus (HCV), a positive-strand enveloped RNA virus belonging to the Flaviviridae family, genus Hepacivirus, causes acute and chronic liver damage. 1 The mechanisms responsible for the tissue injury are poorly understood. 2 HCV often leads to hepatocellular carcinoma and, less frequently, to B-cell non-Hodgkin lymphoma (B-NHL). [3][4][5] HCV is mainly characterized by the failure to generate an effective immune response. Derangement of the B cell immune response has recently been explored by analyses of the size and sequence of complementarity determining region-3 (CDR-3) in the variable diversity joining (VDJ) segment of immunoglobulin heavy chain (IgH), which provide a molecular footprint of the overall B cell receptor (BCR) repertoire. 6 CDR H 3 is the segment of the Ig molecules that most closely interacts with the foreign immunogenic peptides and triggers the adaptive B cell immune response. BCRs of different specificities are generated by different combinations of V, D, and J gene segments to maximize CDR H 3 diversity and to provide the unique specificity of BCR. 7 Because of the lack of an efficient cell culture system for HCV, functions of most virus-encoded proteins have been established by analogy to other viruses and by homology to known proteins. HCV core protein modulates gene transcription, cell proliferation, and cell death. 8 NS3-encoded protein shows numerous interactions with cellular components, including protein-kinases, p53, and histones. 9 NS5A protein has been found to contain a Bcl-2 (B-cell lymphoma-2) homology domain capable of protecting cells against apoptosis. 10 Ability of HCV to prolong the life span of the cells it infects is believed to be of etiological significance, because it enhances the risk of accumulating genetic errors.

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Cited by 11 publications

References 14 publications

Significance of increased expression of decoy receptor 3 in chronic liver disease

Significance of increased expression of decoy receptor 3 in chronic liver disease

Correlation between vitamin D levels and apoptosis in geriatric patients infected with hepatitis C virus genotype 4

HCV-Associated B Cell Clonalities in the Liver Do Not Carry the t(14;18) Chromosomal Translocation *

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