Hepatic Injury from Chronic Hypervitaminosis a Resulting in Portal Hypertension and Ascites

Rm, Russell; Jl, Boyer; Sa, Bagheri; Hruban, Z.

doi:10.1056/nejm197408292910903

Cited by 198 publications

(59 citation statements)

References 18 publications

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“…Some authors suggested that the vitamin A may have stimulated fibrogenesis in the liver lobules in those patients (MUENTER et al, 1971;HRUBAN et al, 1971;RUSSELL et al, 1974). EHRLICH et al (1973) andLEE et al (1973) reported accelerated fibrogenesis also in the skin after administrations of excess doses of vitamin A.…”

Section: Discussionmentioning

confidence: 99%

Effects of Vitamin A Administration upon Ito's Fat-Storing Cells of the Liver in the Carp

Takahashi

Tsubouchi

Kobayashi

1978

Arch. Histol. Jap., Arch. Histol. Jpn

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Section: Discussionmentioning

confidence: 99%

Effects of Vitamin A Administration upon Ito's Fat-Storing Cells of the Liver in the Carp

Takahashi

Tsubouchi

Kobayashi

1978

Arch. Histol. Jap., Arch. Histol. Jpn

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“…It has been shown that vitamin A deficiency in rats potentiates liver fibrosis induced by carbon tetrachloride (CCl 4 ) (Seifert et al, 1994), whereas administration of retinol inhibits CCl 4 -induced fibrosis (Senoo and Wake, 1985) and collagen synthesis by HSC (Shiratori et al, 1987). On the other hand, chronic hypervitaminosis A results in severe liver fibrosis in human by a poorly understood mechanism (Farrell et al, 1977;Russell et al, 1974). Altogether, these findings support a mechanistic link between vitamin A metabolism and the activation of fibrogenic cells.…”

mentioning

confidence: 88%

Cellular Retinol-Binding Protein-1 Expression and Modulation during In Vivo and In Vitro Myofibroblastic Differentiation of Rat Hepatic Stellate Cells and Portal Fibroblasts

Uchio¹,

Tuchweber

Manabe

et al. 2002

Laboratory Investigation

103

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SUMMARY:Cellular retinol-binding protein-1 (CRBP-1) is involved in vitamin A metabolism because it mediates both retinol esterification to retinyl esters and retinol oxidation to retinal and retinoic acid. CRBP-1 is highly expressed in the liver, particularly in hepatic stellate cells (HSC). In this study, we investigated the liver expression of CRBP-1 during experimental fibrogenesis. We also studied the regulation of CRBP-1 expression in cultured HSC and portal fibroblasts, two fibroblastic cell types involved in liver fibrogenesis. Fibrosis was induced in rats by carbon tetrachloride (CCl 4 ) or bile duct ligation. Immunohistochemical staining was performed for CRBP-1 and ␣-smooth muscle (SM) actin, an activation marker of fibrogenic cells. CRBP-1 and ␣-SM actin expression was studied by Western blotting and/or Northern blot in primary cultures of HSC isolated by conventional methods and in portal fibroblasts that were obtained by outgrowth from the biliary tree after enzymatic digestion. In normal liver, contrary to HSC, portal fibroblasts did not express CRBP-1. After CCl 4 injury, CRBP-1 expression was maintained in myofibroblastic ␣-SM actin-positive HSC. After bile duct ligation, portal fibroblasts (which proliferated around ductular structures) acquired expression of both CRBP-1 and ␣-SM actin. During HSC activation in culture, CRBP-1 expression gradually increased until Day 5 when ␣-SM actin expression was obvious. Cultured portal fibroblasts developed both CRBP-1 and ␣-SM actin expression. In both cell populations, transforming growth factor-␤1 treatment increased CRBP-1 expression. Thus, in normal liver, CRBP-1 expression was different among fibroblastic cells, a finding that adds to the concept of heterogeneity of liver fibrogenic cells. Furthermore, during myofibroblastic differentiation, HSC that lost their stores of retinol maintained a high level of CRBP-1 expression, whereas portal fibroblasts acquired CRBP1 expression. Together, these data suggest a correlation between CRBP-1 expression and myofibroblastic differentiation. (Lab Invest 2002, 82:619 -628).

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“…They reported decreased phagocytic and bactericidal activities [109,134]. The amount of lysozyme delivered in secretions was reduced [41,135] as was the amount in lymphocytes [134,136] from vitamin A-deficient children.…”

Section: Vitamin a And Humoral Immunitymentioning

confidence: 99%

Vitamin A Deficiency and Immunity.

Dhur¹,

Galán²,

Herçberg³

1991

J. Clin. Biochem. Nutr.

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Hepatic Injury from Chronic Hypervitaminosis a Resulting in Portal Hypertension and Ascites

Cited by 198 publications

References 18 publications

Effects of Vitamin A Administration upon Ito's Fat-Storing Cells of the Liver in the Carp

Effects of Vitamin A Administration upon Ito's Fat-Storing Cells of the Liver in the Carp

Cellular Retinol-Binding Protein-1 Expression and Modulation during In Vivo and In Vitro Myofibroblastic Differentiation of Rat Hepatic Stellate Cells and Portal Fibroblasts

Vitamin A Deficiency and Immunity.

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