Distribution and localization of caveolin-1 in sinusoidal cells in rat liver

Ogi, Mariko; Yokomori, Hiroaki; Oda, Masaya; Yoshimura, Kazunori; Nomura, Masahiko; Ohshima, Susumu; Akita, Masumi; Toda, Kyoko; Ishii, Hiromasa

doi:10.1007/s007950300004

Cited by 38 publications

(49 citation statements)

References 23 publications

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“…Caveolin-1 is a key structural protein of caveolae and plays a role in the aging process (Cho et al, 2003). Liver fenestrations may possibly be a form of fused caveolae and caveolin-1 has been identified lining the walls of fenestrations (Ogi et al, 2003). Consistent with this report, we found intense peri-sinusoidal expression of caveolin-1 in young healthy livers.…”

Section: Discussionsupporting

confidence: 89%

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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Section: Discussionsupporting

confidence: 89%

Caloric restriction reduces age-related pseudocapillarization of the hepatic sinusoid

Jamieson

Hilmer

Cogger

et al. 2007

Experimental Gerontology

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“…Von Willebrand factor is an endothelial glycoprotein that mediates attachment of platelets after endothelial injury; its upregulation in the LSECs is indicative of a pathophysiological state in these cells. Caveolin-1 is a protein found in fenestrations [20]. Its upregulation has been reported in cirrhosis of the liver [21].…”

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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“…2) was surprising, because the liver has been reported to express only low levels of caveolin-1 36 and the subcellular distribution of caveolin-1 in rat liver has remained controversial. [37][38][39] Therefore, we investigated the exact hepatocellular surface distribution of caveolin-1 in more detail and compared it with established basolateral and canalicular marker proteins as well as with the surface distribution of reggie-1 and reggie-2. As illustrated in Fig.…”

Section: Resultsmentioning

confidence: 99%

ABC-transporters are localized in caveolin-1-positive and reggie-1-negative and reggie-2-negative microdomains of the canalicular membrane in rat hepatocytes

et al. 2008

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The canalicular plasma membrane is constantly exposed to bile acids acting as detergents. Bile acids are essential to mediate release of biliary lipids from the canalicular membrane. Membrane microdomains (previously called lipid rafts) are biochemically defined by their resistance to detergent solubilization at cold temperature. We aimed to investigate the canalicular plasma membrane for the presence of microdomains, which could protect this membrane against the detergent action of bile acids. Highly purified rat liver canalicular plasma membrane vesicles were extracted with 1% Triton X-100 or 1% Lubrol WX at 4°C and subjected to flotation through sucrose step gradients. Both detergents yielded detergent-resistant membranes containing the microdomain markers alkaline phosphatase and sphingomyelin. However, cholesterol was resistant to Lubrol WX solubilization, whereas it was only marginally resistant to solubilization by Triton X-100. The microdomain marker caveolin-1 was localized to the canalicular plasma membrane domain and was resistant to Lubrol WX, but to a large extent solubilized by Triton X-100. The two additional microdomain markers, reggie-1 and reggie-2, were localized to the basolateral and canalicular plasma membrane and were partially resistant to Lubrol WX but resistant to Triton X-100. The canalicular transporters bile salt export pump, multidrug resistance protein 2, multidrug resistance-associated protein 2, and Abcg5 were largely resistant to Lubrol WX but were solubilized by Triton X-100. Conclusion: These results indicate the presence of two different types of microdomains in the canalicular plasma membrane: "Lubrol-microdomains" and "Triton-microdomains". "Lubrol-microdomains" contain the machinery for canalicular bile formation and may be the starting place for canalicular lipid secretion. (HEPATOLOGY 2009;49:1673-1682

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Distribution and localization of caveolin-1 in sinusoidal cells in rat liver

Cited by 38 publications

References 23 publications

Caloric restriction reduces age-related pseudocapillarization of the hepatic sinusoid

Caloric restriction reduces age-related pseudocapillarization of the hepatic sinusoid

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

ABC-transporters are localized in caveolin-1-positive and reggie-1-negative and reggie-2-negative microdomains of the canalicular membrane in rat hepatocytes

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