β‐Carotene storage, conversion to retinoic acid, and induction of the lipocyte phenotype in hepatic stellate cells

Martucci, Renata Brum; Ziulkoski, Ana Luíza; Fortuna, Vitor; Guaragna, Regina Maria Vieira da Costa; Guma, Fátima Costa Rodrigues; Trugo, L.C.; Borojević, Radovan

doi:10.1002/jcb.20073

Cited by 32 publications

(25 citation statements)

References 42 publications

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“…Indeed, some nonintestinal viral infections also induce 4 7 + T cells 103 and there may be constitutive sources of RA in the lung mucosa 104 and liver. 105 Also, it remains to be determined whether RA synthesis can be induced in nonintestinal tissues under inflammatory or infectious conditions and whether there are additional RA-independent mechanisms of gut-homing imprinting. 106 It is also unknown how IgA-ASCs are imprinted to home to mucosal compartments other than the small bowel.…”

Section: Mechanisms Of Imprinting Of Gut-homing B Cells and Ascmentioning

confidence: 99%

Differentiation and homing of IgA-secreting cells

2008

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Most antibody-secreting cells (ASCs) in mucosal tissues produce immunoglobulin A (IgA), the most abundant immunoglobulin in the body and the main class of antibody found in secretions. IgA-ASCs differentiate in the mucosal-associated lymphoid tissues and are usually considered as a homogeneous population of cells. However, IgA-ASCs that travel to the small intestine have unique characteristics in terms of their migratory requirements. These IgA-ASCs require the homing molecules alpha4beta7 and CCR9 to interact with their ligands, mucosal addressin cell adhesion molecule-1 and CCL25, which are constitutively expressed in the small intestine. Indeed, recent work has shown that IgA-ASCs specific for the small bowel are generated under different conditions as compared with IgA-ASCs in other mucosal compartments. Moreover, the mechanisms inducing IgA class switching may also vary according to the tissue where IgA-ASCs differentiate. Here we describe the mechanisms involved in the differentiation of IgA-ASCs in mucosal compartments, in particular those involved in the generation of gut-homing IgA-ASCs.

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Section: Mechanisms Of Imprinting Of Gut-homing B Cells and Ascmentioning

confidence: 99%

Differentiation and homing of IgA-secreting cells

2008

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“…Activated HSCs respond to exogenous retinoids in culture (Hellemans et al 2004;Martucci et al 2004;Vogel et al 2000). Studies have shown that supplementation of cultured HSCs with ATROH prevents the activation of HSCs, inhibits transdifferentiation, and promotes the lipofibroblastic vitamin-A-storing phenotype (Vogel et al 2000;Fortuna et al 2003;Hellemans et al 2004).…”

Section: Introductionmentioning

confidence: 95%

Transdifferentiation of vocal-fold stellate cells and all-trans retinol-induced deactivation

2005

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The maculae flavae of the human vocal folds include dense extracellular matrices and compacted cells with a stellate morphology. These vocal-fold stellate cells are thought to participate in the metabolism of extracellular matrices essential in maintaining vocal-fold viscoelasticity required for phonation. We have isolated and cultured these new cells and have tested the hypothesis that they maintain a distinct cellular and biochemical phenotype. We have compared proliferation rates, changes on immunophenotype, and intracellular lipid and vitamin A storage. Vocal-fold stellate cells undergo culture-induced transdifferentiation to a myofibroblast-like phenotype with an altered phenotype resembling, but not identical to, activated hepatic and pancreatic stellate cells. Our results reveal that these cells are capable of responding to exogenous all-trans retinol in culture. Exposure to this synthetic co-factor causes deactivation characterized by decreased proliferation, loss of the activated stellate cell marker, alpha-smooth muscle actin, and restoration of intracellular lipid and vitamin A metabolite storage. These data establish a new and distinct cellular target for future investigations of the viscoelastic properties of the vocal-fold mucosa during normal phonation, aging, vocal-fold scarring, laryngeal fibrosis, and myofibroblastoma.

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“…Along with retinoid stores, liver has also been shown to accumulate significant amount of carotenoids under normal physiological conditions. In vivo and in vitro models have shown that both hepatocytes and hepatic stellate cells accumulate carotenoid [19–21]. Hepatic accumulation of β-carotene has been observed in both the BCO1 and BCO2 -deficient mice [22,23].…”

Section: Introductionmentioning

confidence: 99%

Cellular localization of β-carotene 15,15′ oxygenase-1 (BCO1) and β-carotene 9′,10′ oxygenase-2 (BCO2) in rat liver and intestine

Raghuvanshi

Reed

Blaner

et al. 2015

Archives of Biochemistry and Biophysics

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The intestine and liver are crucial organs for vitamin A uptake and storage. Liver accounts for 70% of total body retinoid stores. Vitamin A deficiency (VAD) is a major micronutrient deficiency around the world. The provitamin A carotenoid, β-carotene, is a significant source of vitamin A in the diet. β-Carotene 15,15′ oxygenase-1 (BCO1) and β-carotene 9′,10′ oxygenase-2 (BCO2) are the two known carotenoid cleavage enzymes in humans. BCO1 and BCO2 are highly expressed in liver and intestine. Hepatocytes and hepatic stellate cells are two main cell types involved in the hepatic metabolism of retinoids. Stellate-like cells in the intestine also show ability to store vitamin A. Liver is also known to accumulate carotenoids, however, their uptake, retention and metabolism in specific liver and intestinal cell types is still unknown. Hence, we studied the cellular and subcellular expression and localization of BCO1 and BCO2 proteins in rat liver and intestine. We demonstrate that both BCO1 and BCO2 proteins are localized in hepatocytes and mucosal epithelium. We also show that BCO1 is also highly expressed in hepatic stellate cells (HSC) and portal endothelial cells in liver. At the subcellular level in liver, BCO1 is found in cytosol, while BCO2 is found in mitochondria. In intestine, immunohistochemistry showed strong BCO1 immunoreactivity in the duodenum, particularly in Brunner’s glands. Both BCO1 and BCO2 showed diffuse presence along epithelia with strong immunoreactivity in endothelial cells and in certain epithelial cells which warrant further investigation as possible intestinal retinoid storage cells.

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β‐Carotene storage, conversion to retinoic acid, and induction of the lipocyte phenotype in hepatic stellate cells

Cited by 32 publications

References 42 publications

Differentiation and homing of IgA-secreting cells

Differentiation and homing of IgA-secreting cells

Transdifferentiation of vocal-fold stellate cells and all-trans retinol-induced deactivation

Cellular localization of β-carotene 15,15′ oxygenase-1 (BCO1) and β-carotene 9′,10′ oxygenase-2 (BCO2) in rat liver and intestine

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