Non-classical Transcriptional Activity of Retinoic Acid

Noy, Noa

doi:10.1007/978-94-024-0945-1_7

Cited by 17 publications

(17 citation statements)

References 143 publications

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“…Noy and colleagues, in a series of publications, proposed that all-trans-retinoic acid acting transcriptionally through PPARβ/δ modulates adipocyte differentiation and responses and whole body adiposity (Berry and Noy, 2009;Berry et al, 2010;Berry et al, 2013;Noy, 2013;Noy, 2016a). These authors proposed an explanation for why all-trans-retinoic acid can block preadipocyte differentiation into adipocytes but yet be needed for mediating retinoic acid-dependent transcriptional signaling in mature adipocytes.…”

Section: B Vitamin a Vitamin A-related Proteins And Adipose Biologymentioning

confidence: 99%

Vitamin A signaling and homeostasis in obesity, diabetes, and metabolic disorders

Blaner

2019

Pharmacology & Therapeutics

200

174

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Much evidence has accumulated in the literature over the last fifteen years that indicates vitamin A has a role in metabolic disease prevention and causation. This literature proposes that vitamin A can affect obesity development and the development of obesity-related diseases including insulin resistance, type 2 diabetes, hepatic steatosis and steatohepatitis, and cardiovascular disease. Retinoic acid, the transcriptionally active form of vitamin A, accounts for many of the reported associations. However, a number of proteins involved in vitamin A metabolism, including retinolbinding protein 4 (RBP4) and aldehyde dehydrogenase 1A1 (ALDH1A1, alternatively known as retinaldehyde dehydrogenase 1 or RALDH1), have also been identified as being associated with metabolic disease. Some of the reported effects of these vitamin A-related proteins are proposed to be independent of their roles in assuring normal retinoic acid homeostasis. This review will consider both human observational data as well as published data from molecular studies undertaken in rodent models and in cells in culture. The primary focus of the review will be on the effects that vitamin A per se and proteins involved in vitamin A metabolism have on adipocytes, adipose tissue biology, and adipose-related disease, as well as on early stage liver disease, including non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH).

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Section: B Vitamin a Vitamin A-related Proteins And Adipose Biologymentioning

confidence: 99%

Vitamin A signaling and homeostasis in obesity, diabetes, and metabolic disorders

Blaner

2019

Pharmacology & Therapeutics

200

174

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“…Partitioning RA between RARs and PPARβ/δ is governed by different intracellular lipid-binding proteins: CRABP2 selectively delivers RA to nuclear RARs and a fatty acid binding protein, FABP5, delivers RA from the cytosol to nuclear PPARβ/δ. Consequently, since RARs and PPARβ/δ regulate the expression of distinct sets of genes, RA stimulates different cellular responses depending on whether RARs or PPARβ/δ are activated [ 64 , 65 ].…”

Section: Vitamin a Metabolism And Retinoid Signallingmentioning

confidence: 99%

Vitamin A Deficiency and the Lung

et al. 2018

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Vitamin A (all-trans-retinol) is a fat-soluble micronutrient which together with its natural derivatives and synthetic analogues constitutes the group of retinoids. They are involved in a wide range of physiological processes such as embryonic development, vision, immunity and cellular differentiation and proliferation. Retinoic acid (RA) is the main active form of vitamin A and multiple genes respond to RA signalling through transcriptional and non-transcriptional mechanisms. Vitamin A deficiency (VAD) is a remarkable public health problem. An adequate vitamin A intake is required in early lung development, alveolar formation, tissue maintenance and regeneration. In fact, chronic VAD has been associated with histopathological changes in the pulmonary epithelial lining that disrupt the normal lung physiology predisposing to severe tissue dysfunction and respiratory diseases. In addition, there are important alterations of the structure and composition of extracellular matrix with thickening of the alveolar basement membrane and ectopic deposition of collagen I. In this review, we show our recent findings on the modification of cell-junction proteins in VAD lungs, summarize up-to-date information related to the effects of chronic VAD in the impairment of lung physiology and pulmonary disease which represent a major global health problem and provide an overview of possible pathways involved.

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“…In our study, we documented the increased CRBPI expression in human skin psoriatic lesions and the greater severity of lesions in CRBPI-knockout mice in an imiquimod-induced model of psoriasis. CRBPI is a small cytosolic 15KDa protein widely expressed and evolutionarily conserved in many tissues [7]. CRBPI acts as chaperone protein and regulates uptake and subsequent esterification of retinol and its bioavailability [9, 10].…”

Section: Discussionmentioning

confidence: 99%

“…Risk and genetic factors interact with environmental agents such as drugs, stress or infections [1, 3, 5, 6] but still many aspects of the pathogenesis of psoriasis remain partially unknown. Retinoids regulate proliferation and differentiation of skin keratinocytes [7]. Cellular retinol binding protein I (CRBPI) is a cytosolic carrier of retinol essential for its homeostasis [8–10].…”

Section: Introductionmentioning

confidence: 99%

Expression and potential role of cellular retinol binding protein I in psoriasis

et al. 2018

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Psoriasis is a diffuse chronic skin disorder characterized from accelerated epidermal turnover and inflammatory cell infiltrate. Retinoids influence keratinocyte proliferation and differentiation as well as inflammatory response. Cellular retinol binding protein (CRBPI) regulates intracellular vitamin A bioavailability and contributes to maintain skin homeostasis. The aim of present study was to investigate the expression of CRBPI and its role in the pathogenesis of skin psoriasis. Immunohistochemistry revealed more diffuse and increased CRBPI expression in all epidermal layers of human psoriatic lesions except in the stratum corneum. An imiquimod-induced psoriatic-like model documented the increase of skin lesional area and severity index score as well as of the severity of microscopic features as parakeratosis, papillomatosis and spongiosis in CRBPI-knockout compared to wild-type mice, associated to the increased keratinocyte CK17 and Ki-67 expression and the reduction of CK1, CRABPII and RXRα. Gene array of imiquimod-induced psoriatic skin documented the greater up-regulation of EGF/PDGF-related genes and down-regulation of EGR1 and pro-inflammatory IL-related genes in CRBPI-knockout compared to wild-type mice. Finally, CRBPI transfection in HaCaT cells increased AKT and NF-κB-related genes and proteins and down-regulated IL-2, IL-6 and IL-8 pro-inflammatory signalling. Although not recognized as a psoriatic susceptibility gene in our cohort of patients, the present data strongly supported the potential role of CRBPI to sustain keratinocyte proliferation and differentiation and to counteract pro-inflammatory genes expression in psoriatic lesions.

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Non-classical Transcriptional Activity of Retinoic Acid

Cited by 17 publications

References 143 publications

Vitamin A signaling and homeostasis in obesity, diabetes, and metabolic disorders

Vitamin A signaling and homeostasis in obesity, diabetes, and metabolic disorders

Vitamin A Deficiency and the Lung

Expression and potential role of cellular retinol binding protein I in psoriasis

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