The effects of oxidative stress on the liver sieve

Cogger, Victoria C.; Müller, Michael; Fraser, Robin; McLean, Allan J.; Khan, Jameel Ahmad; Couteur, David G. Le

doi:10.1016/j.jhep.2004.04.034

Cited by 69 publications

(53 citation statements)

References 48 publications

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“…Das et al showed that nine months was required before overt liver injury was observed in response to high levels of arsenic and that this injury was associated with increased oxidative damage and cytokine release (Das et al, 2005). Capillarization has been shown to occur with aging, an effect that may be caused by progressive oxidative injury to LSEC (Hilmer et al, 2005;Cogger et al, 2004). The data in Fig.…”

Section: Discussionmentioning

confidence: 97%

“…Liver angiogenesis in general is recognized as an important factor in the pathogenesis not only for portal fibrosis, but also for portal hypertension and progression of hepatocellular carcinomas (Tsuneyama et al, 2003;Ward et al, 2004;Semela et al, 2004;Moreau, 2005;Fernandez et al, 2005). Finally, liver capillarization impacts the systemic vasculature by decreasing liver metabolism of lipids, lipoproteins, and glucose to promote atherogenesis in response to environmental stresses and aging (Braet et al, 2002;Cogger et al, 2004;Hilmer et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Low level arsenic promotes progressive inflammatory angiogenesis and liver blood vessel remodeling in mice

Straub

Stolz

Vin

et al. 2007

Toxicology and Applied Pharmacology

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The vascular effects of arsenic in drinking water are global health concerns contributing to human disease worldwide. Arsenic targets the endothelial cells lining blood vessels and endothelial cell activation or dysfunction may underlie the pathogenesis of both arsenic-induced vascular diseases and arsenic-enhanced tumorigenesis. The purpose of the current studies was to demonstrate that exposing mice to drinking water containing environmentally relevant levels of arsenic promoted endothelial cell dysfunction and pathologic vascular remodeling. Increased angiogenesis, neovascularization, and inflammatory cell infiltration was observed in Matrigel plugs implanted in C57BL/6 mice following 5 week exposures to 5-500 ppb arsenic (Soucy et al., 2005). Therefore, functional in vivo effects of arsenic on endothelial cell function and vessel remodeling in an endogenous vascular bed were investigated in the liver. Liver sinusoidal endothelial cells (LSEC) became progressively defenestrated and underwent capillarization to decrease vessel porosity following exposure to 250 ppb arsenic for 2 weeks. Sinusoidal expression of PECAM-1 and laminin-1 proteins, a hallmark of capillarization, was also increased by 2 weeks of exposure. LSEC caveolin-1 protein and caveolae expression were induced after 2 weeks of exposure indicating a compensatory change. Likewise, CD45/CD68 positive inflammatory cells did not accumulate in the livers until after LSEC porosity was decreased; indicating that inflammation is a consequence and not a cause of the arsenic-induced LSEC phenotype. The data demonstrate that the liver vasculature is an early target of pathogenic arsenic effects and that the mouse liver vasculature is a sensitive model for investigating vascular health effects of arsenic.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Low level arsenic promotes progressive inflammatory angiogenesis and liver blood vessel remodeling in mice

Straub

Stolz

Vin

et al. 2007

Toxicology and Applied Pharmacology

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“…In some cases, the stellate cells appeared to occlude fenestrations and potentially increase the effective diffusional distance for substrate transfer between the sinusoidal lumen and the space of Disse. Oxidative stress, which is increased in diabetes [29], also has marked effects on the structure of the LSECs [30,31].…”

Section: Discussionmentioning

confidence: 99%

Alterations in liver sinusoidal endothelium in a baboon model of type 1 diabetes

et al. 2007

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Aims/hypothesis Diabetes mellitus is associated with extensive vascular pathology, yet little is known about its longterm effects on liver sinusoidal endothelial cells (LSECs).Potential diabetic changes in LSECs are important because of the role played by fenestrations in the LSECs in hepatic disposition of lipoproteins. Materials and methods Surgical liver biopsies for electron microscopy and immunohistochemistry were obtained from baboons with long-standing streptozotocin-induced, insulin-treated diabetes mellitus and compared with those from age-matched control animals. Results There was an increase in the thickness of LSECs (170±17 vs 123±10 nm, p<0.01). Fenestrations in LSECs, as determined by overall porosity, were markedly reduced (1.4±0.1% vs 2.6±0.2%, p<0.01). Increased numbers of stellate cells were seen on electron microscopy, and this finding was corroborated by increased smooth muscle actin expression. Diabetes mellitus was also associated with increased endothelial production of von Willebrand factor and caveolin-1. Conclusions/interpretation Diabetes mellitus in the nonhuman primate is associated with marked changes in LSECs, including a reduction in fenestrations. Such changes provide an additional and novel mechanism for impaired hepatic lipoprotein clearance and post-prandial hyperlipidaemia in diabetes mellitus.

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“…The liver sinusoidal endothelium is exquisitely sensitive to oxidative stress Cogger et al, 2004) and other toxic insults (McCuskey, 2006). Thus, it is plausible that the structure of the liver sinusoidal endothelium may be profoundly influenced by the quantity of the dietary load, with its concomitant oxidants delivered via the portal vein.…”

Section: Introductionmentioning

confidence: 99%

Caloric restriction reduces age-related pseudocapillarization of the hepatic sinusoid

Jamieson

Hilmer

Cogger

et al. 2007

Experimental Gerontology

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Age-related changes in the hepatic sinusoid, called pseudocapillarization, may contribute to the pathogenesis of dyslipidaemia. Caloric restriction (CR) is a powerful model for the study of aging because it extends lifespan. We assessed the effects of CR on the hepatic sinusoid to determine whether pseudocapillarization is preventable and hence a target for the prevention of age-related dyslipidemia. Livers from young (6 months) and old (24 months) CR and ad libitum fed (AL) F344 rats were examined using electron microscopy and immunohistochemistry. In old age, there was increased thickness of the liver sinusoidal endothelium and reduced endothelial fenestration porosity. In old CR rats, endothelial thickness was less and fenestration porosity was greater than in old AL rats. Immunohistochemistry showed that CR prevented age-related decrease in caveolin-1 expression and increase in peri-sinusoidal collagen IV staining, but did not alter the age-related increase of von Willebrand's factor. CR reduces age-related pseudocapillarization of the hepatic sinusoid and correlates with changes in caveolin-1 expression.

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The effects of oxidative stress on the liver sieve

Cited by 69 publications

References 48 publications

Low level arsenic promotes progressive inflammatory angiogenesis and liver blood vessel remodeling in mice

Low level arsenic promotes progressive inflammatory angiogenesis and liver blood vessel remodeling in mice

Alterations in liver sinusoidal endothelium in a baboon model of type 1 diabetes

Caloric restriction reduces age-related pseudocapillarization of the hepatic sinusoid

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