Studies from a number of laboratories have provided information on the temporal and spatial expression of a variety of extracellular matrix (ECM) components in the developing liver and insight into their potential roles in hepatogenesis. Collagen type IV and laminin are present in the basement membr
Vitamin A deficiency injures liver parenchyma and alters the expression of hepatic extracellular matrix
✍ Scribed by Rossana Pérez Aguilar; Susana Genta; Liliana Oliveros; Ana Anzulovich; María Sofía Giménez; Sara S. Sánchez
- Publisher
- John Wiley and Sons
- Year
- 2009
- Tongue
- English
- Weight
- 532 KB
- Volume
- 29
- Category
- Article
- ISSN
- 0260-437X
- DOI
- 10.1002/jat.1399
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✦ Synopsis
Abstract
Vitamin A is an essential lipid‐soluble nutrient that is crucial for morphogenesis and adult tissue maintenance. The retinoid homeostasis in the liver depends on a regular supply of vitamin A from an adequate dietary intake to preserve the normal organ structure and functions. This study focuses on the effect of vitamin A deficiency on the morphology and extracellular proteins expression of the liver in adult Wistar rats. Animals were fed with a normal (control group) or deficient vitamin A diet for 3 months. At the end of the experimental period, histological examination of the livers under light and electron microscopy revealed that vitamin A deficiency produced a loss of hepatocyte cord disposition with an irregular parenchymal organization. Abundant fat droplets were present in the cytoplasm of the hepatocytes. Elongated myofibroblastic‐like cells with an irregular cytoplasmic process and without lipid droplets could be seen at the perisinusoidal space, where an elevated intensity of alpha smooth muscle actin (α‐SMA) was observed. These results suggest that an activation of hepatic stellate cells (HSCs) occurred. Moreover, immunochemical methods revealed that vitamin A deficiency led to an increased expression of hepatic fibronectin, laminin and collagen type IV. We propose that vitamin A deprivation caused liver injury and that HSCs underwent a process of activation in which they produced α‐SMA and synthesized extracellular components. These changes may be a factor predisposing to liver fibrosis. In consequence, vitamin A deprivation could affect human and animal health. Copyright © 2008 John Wiley & Sons, Ltd.
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