Phenotypic and Functional Differences between Human Liver Cancer Endothelial Cells and Liver Sinusoidal Endothelial Cells

Wu, Lian Qiu; Zhang, Wen Jian; Niu, Ji Xiao; Ye, Li Ya; Liu, Yang; Grau, Georges E.; Lou, Jinning

doi:10.1159/000109079

Cited by 32 publications

(17 citation statements)

References 29 publications

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“…LSECs, derived from both the resident LSEC population and from circulating precursors, respond to signals within the microenvironment such as vascular endothelial growth factor (VEGF) and fibroblast growth factor to change their proliferative state and to express different adhesion molecules, resulting in sprouting new vasculature [89–91]. This in turn results in enhanced blood supply to injured liver tissue and tumor tissue.…”

Section: Cellular Components Of the Hbv-associated Hcc Environmentmentioning

confidence: 99%

The hepatitis B virus-associated tumor microenvironment in hepatocellular carcinoma

Yang

Markowitz

Wang

2014

National Science Review

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In contrast to a majority of cancer types, the initiation of hepatocellular carcinoma (HCC) is intimately associated with a chronically diseased liver tissue, with one of the most prevalent etiological factors being hepatitis B virus (HBV). Transformation of the liver in HBV-associated HCC often follows from or accompanies long-term symptoms of chronic hepatitis, inflammation and cirrhosis, and viral load is a strong predictor for both incidence and progression of HCC. Besides aiding in transformation, HBV plays a crucial role in modulating the accumulation and activation of both cellular components of the microenvironment, such as immune cells and fibroblasts, and non-cellular components of the microenvironment, such as cytokines and growth factors, markedly influencing disease progression and prognosis. This review will explore some of these components and mechanisms to demonstrate both underlying themes and the inherent complexity of these interacting systems in the initiation, progression, and metastasis of HBV-positive HCC.

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Section: Cellular Components Of the Hbv-associated Hcc Environmentmentioning

confidence: 99%

The hepatitis B virus-associated tumor microenvironment in hepatocellular carcinoma

Yang

Markowitz

Wang

2014

National Science Review

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“…The study protocol was examined and approved by the Ethical Committee for Research in Humans of China-Japan Friendship Hospital. The method for the isolation of microvascular endothelial cells was previously described (Wu et al, 2008). In brief, the tissues were cut into 2 mm×2 mm pieces and then digested in 10 mL of 0.2% collagenase type I (Sigma, USA) for 20 min at 37°C.…”

Section: Isolation and Purification Of Microvascular Endothelial Cellmentioning

confidence: 99%

Platelet-mediated adhesion facilitates leukocyte sequestration in hypoxia-reoxygenated microvessels

Zheng

Cao

Zhang

et al. 2016

Sci. China Life Sci.

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Leukocyte transendothelial migration and sequestration are two distinct outcomes following leukocyte adhesion to endothelium during ischemia-reperfusion injury, in which platelets may play a pivotal role. In the present study, we established an in vitro hypoxia-reoxygenation model to mimic ischemia-reperfusion injury and found platelet pre-incubation significantly increased leukocyte adhesion to endothelial cells after hyoxia-reoxygenation (over 67%). Blockade of endothelial-cell-expressed adhesion molecules inhibited leukocyte direct adhesion to endothelial cells, while platelet-mediated leukocyte adhesion was suppressed by blockade of platelet-expressed adhesion molecules. Further experiments revealed platelets acted as a bridge to mediate leukocyte adhesion, and platelet-mediated adhesion was the predominant pattern in the presence of platelets. However, platelet pre-incubation significantly suppressed leukocyte transendothelial migration after hypoxia-reoxygenation (over 31%), which could be aggravated by blockade of endothelial-cell-expressed adhesion molecules, but alleviated by blockade of platelet-expressed adhesion molecules. This would indicate that platelet-mediated adhesion disrupted leukocyte transendothelial migration. An in vivo mesenteric ischemia-reperfusion model demonstrated leukocyte transfusion alone caused mild leukocyte adhesion to reperfused vessels and subsequent leukocyte infiltration, while simultaneous leukocyte and platelet transfusion led to massive leukocyte adhesion and sequestration within reperfused microvessels. Our studies revealed platelets enhanced leukocyte adhesion to endothelial cells, but suppressed leukocyte transendothelial migration. Overall, this leads to leukocyte sequestration in hypoxia-reoxygenated microvessels. adhesion, endothelial cells, hypoxia-reoxygenation, leukocytes, platelets, transendothelial migration Citation:Zheng, S., Cao, Y., Zhang, W., Liu, H., You, J., Yin, Y., Liu, J., and Li, C. (2016). Platelet-mediated adhesion facilitates leukocyte sequestration in hypoxia-reoxygenated microvessels . Sci China Life Sci 59, 299 -311.

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“…A LSEC cell line has been generated from immortalized cells of human liver endothelial cell primary cultures [138]. Cells do not transform and express phenotypic markers of primary cultures [139] and respond to inflammatory molecules such as TNF [140] and to hypoxia/reoxygenation stress by inducing necrosis and apoptosis [141]. Incubation of virulent trophozoites of E. histolytica with LSEC interfered with host cell adhesion signaling and leads to diminished adhesion and target cell death.…”

Section: Models Of Pathogenesismentioning

confidence: 99%

Molecular Basis of Pathogenesis in Amoebiasis

Saha

Gaurav

Bhattacharya

et al. 2015

Curr Clin Micro Rpt

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Amoebiasis is one of the major public health problems in developing countries. In spite of the availability of an effective drug and absence of overt drug resistance, the disease is still prevalent among large population and spread over a number of countries. It is caused by the protist parasite Entamoeba histolytica that essentially infects humans, though other species that infect a few animals have been reported. A number of molecular techniques have recently been developed. These have helped in understanding biological processes in E. histolytica and in the identification of key molecules that are involved in amoebic virulence and invasion. Moreover, developments in the area of disease and invasion models have allowed understanding of these processes at molecular level and circumvented lack of a good animal model of amoebiasis. All these knowledge will help us to design better therapeutics and allow us to control this important disease.

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Phenotypic and Functional Differences between Human Liver Cancer Endothelial Cells and Liver Sinusoidal Endothelial Cells

Cited by 32 publications

References 29 publications

The hepatitis B virus-associated tumor microenvironment in hepatocellular carcinoma

The hepatitis B virus-associated tumor microenvironment in hepatocellular carcinoma

Platelet-mediated adhesion facilitates leukocyte sequestration in hypoxia-reoxygenated microvessels

Molecular Basis of Pathogenesis in Amoebiasis

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