Lab

Lab Invest 1996, 74:265–278.PubMed 25. Desmoulière A, Darby I, Monte Alto Costa A, Raccurt M, Tuchweber B, Sommer P, Gabbiani F: Extracellular

matrix deposition, lysyl oxydase expression, and myofibroblastic differentiation during the initial stages of cholestatic fibrosis in the rat. Lab Invest 1997, 76:765–778.PubMed 26. Lamireau T, Dubuisson L, Lepreux S, Bioulac-Sage P, Fabre M, Rosenbaum J, Desmoulière A: Abnormal hepatic expression of fibrillin-1 in children with cholestasis. Am J Surg Pathol 2002, 26:637–646.CrossRefPubMed 27. Blomhoff R, Wake K: Perisinusoidal stellate cells of the liver: important roles in retinol metabolism and fibrosis. FASEB J 1991, 5:271–277.PubMed 28. Enzan H, Himeno H, Hiroi M, Kiyoku H, Saibara T, Onishi S: Development of MS-275 hepatic sinusoidal structure with special reference to the Ito cells. Microsc Res Tech 1997, 39:336–349.CrossRefPubMed 29. Leo M, Ahmed S, Aleynik

S, Siegel J, Kasmin F, Lieber C: Carotenoids and tocopherols in various hepatobiliary conditions. J Hepatol 1995, 23:550–556.CrossRefPubMed 30. Hadlock F, Deter R, Harrist R, Park S: Estimating fetal age: computer-assisted analysis of multiple fetal growth parameters. Radiology. 1984,152(2):497–501.PubMed 31. Van Beneden K, Geers C, Van Grunsven L, Pauwels M, Desmoulière A, Verbeelen D, Geerts A, Branden C: CRBP-1 in the renal 3-deazaneplanocin A tubulointerstitial compartment of heathly rats and rats with renal fibrosis. Nephrol Dial Transplant 2008, 23:3464–3471.CrossRefPubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions JV participated in the histological experiments. FPN gave a fetopathology’s BIBW2992 in vivo expertise. CC participated in the histological experiments. DC gave a fetopathology’s expertise. CC participated in the design of immunohistochemical study. JR gave his expertise on fibrogenesis. CB and PBS gave a hepatopathology’s expertise. SL was responsible for the conception, performed the immunohistochemical study and wrote the manuscript. All authors have read and approved the final manuscript.”
“Background It has been postulated that

ethanol primarily targets hepatic sinusoidal and perisinusoidal cells [1]. In experimental models and in human studies, plasma hyaluronic acid levels are elevated in alcoholic liver injury, which may reflect a diminished hepatic clearance by liver Thymidine kinase sinusoidal endothelial cells [2–4]. Chronic ethanol exposure leads to defenestration in liver sinusoidal endothelial cells which is paralleled by the deposition of a basal lamina [5]. Subsequently, capillarization of hepatic sinusoids further impairs microcirculatory exchange of nutrients and the clearance of waste products, enhances tissue fibrosis, and will affect the hepatic parenchyma and its metabolism. Whereas this sequence of events has been corroborated by several studies, it is not well established to which extent a single administration of ethanol affects liver sinusoidal endothelial cells.

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