Cutaneous Lesions Associated With a Deficiency in Vitamin a in Man

Frazier, Chester N.; Hu, Ch'uan-K'uei

doi:10.1001/archinte.1931.00150030158012

Cited by 136 publications

(14 citation statements)

References 4 publications

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“…The profound effects of vitamin A on epidermis have been known for over 60 years (Frazier and t Hu, 1931). Both in vivo and in vitro, retinoic acid (RA) deficiency causes hyperkeratosis and promotes differentiation of epidermal keratinocytes, whereas an excess of RA prevents keratinization and keeps keratinocytes in a basal layer-like phenotype (Fuchs and Green, 1981;Gilfix and Eckert, 1985;Nagae et al, 1987;Asselineau et aL., 1989).…”

Section: Introductionmentioning

confidence: 99%

Nuclear receptors for retinoic acid and thyroid hormone regulate transcription of keratin genes.

et al. 1990

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In the epidermis, retinoids regulate the expression of keratins, the intermediate filament proteins of epithelial cells. We have cloned the 5' regulatory regions of four human epidermal keratin genes, K#5, K#6, K#10, and K#14, and engineered constructs in which these regions drive the expression of the CAT reporter gene. By co-transfecting the constructs into epithelial cells along with the vectors expressing nuclear receptors for retinoic acid (RA) and thyroid hormone, we have demonstrated that the receptors can suppress the promoters of keratin genes. The suppression is ligand dependent; it is evident both in established cell lines and in primary cultures of epithelial cells. The three RA receptors have similar effects on keratin gene transcription. Our data indicate that the nuclear receptors for RA and thyroid hormone regulate keratin synthesis by binding to negative recognition elements in the upstream DNA sequences of the keratin genes. RA thus has a twofold effect on epidermal keratin expression: qualitatively, it regulates the regulators that effect the switch from basal cell-specific keratins to differentiation-specific ones; and quantitatively, it determines the level of keratin synthesis within the cell by direct interaction of its receptors with the keratin gene promoters.

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Section: Introductionmentioning

confidence: 99%

Nuclear receptors for retinoic acid and thyroid hormone regulate transcription of keratin genes.

et al. 1990

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“…Vitamin A (retinol) is an important nutrient for adult health 1,2 and embryonic development 3,4 . Early studies identified active metabolites of vitamin A, such as 11- cis -retinaldehyde (a light-absorbing molecule that is important for vision) 5 and all- trans -retinoic acid (RA; commonly known as retinoic acid) 6 .…”

mentioning

confidence: 99%

Mechanisms of retinoic acid signalling and its roles in organ and limb development

Cunningham

Duester

2015

Nat Rev Mol Cell Biol

476

474

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Retinoic acid (RA) signalling has a central role during vertebrate development. RA synthesized in specific locations regulates transcription by interacting with nuclear RA receptors (RARs) bound to RA response elements (RAREs) near target genes. RA was first implicated in signalling on the basis of its teratogenic effects on limb development. Genetic studies later revealed that endogenous RA promotes forelimb initiation by repressing fibroblast growth factor 8 (Fgf8). Insights into RA function in the limb serve as a paradigm for understanding how RA regulates other developmental processes. In vivo studies have identified RAREs that control repression of Fgf8 during body axis extension or activation of homeobox (Hox) genes and other key regulators during neuronal differentiation and organogenesis.

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“…Vitamin A and its derivatives (retinoids) are critically important in the development and maintenance of multiple tissues, including skin and hair, as shown by the detrimental effects of vitamin A deficiency (Wolbach and Howe, 1925;Frazier and Hu, 1931). These observations have led to the widespread use of retinoids in various skin disorders (Stuttgen, 1986).…”

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confidence: 99%

Hair Cycle-Specific Immunolocalization of Retinoic Acid Synthesizing Enzymes Aldh1a2 and Aldh1a3 Indicate Complex Regulation

Everts

King

Sundberg

et al. 2004

Journal of Investigative Dermatology

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Retinoic acid has long been known to alter skin and hair growth but an exact mechanism is unclear. This study was performed to examine the sites of endogenous retinoic acid synthesis in the cycling hair follicle to better understand the role retinoic acid plays in this process. Retinal dehydrogenases (Aldh1a1, 2, and 3, formerly Raldh 1, 2, and 3) are the enzymes responsible for the last step in retinoic acid synthesis. Immunohistochemistry was performed on adult C57BL/6J mouse skin sections with antibodies against Aldh1a2 and Aldh1a3. Aldh1a2 expression was seen primarily in the outer root sheath and basal/spinous layer during all stages of the hair cycle, and in the bulge during anagen and early catagen, whereas Aldh1a3 expression was primarily in the dermal papilla, pre-cortex, and hair shaft during mid-late anagen. The expression patterns of these two similar retinoic acid synthesizing enzymes at specific follicular sites suggest that they mediate and are regulated by different epithelial proliferation and differentiation signaling pathways.

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Cutaneous Lesions Associated With a Deficiency in Vitamin a in Man

Cited by 136 publications

References 4 publications

Nuclear receptors for retinoic acid and thyroid hormone regulate transcription of keratin genes.

Nuclear receptors for retinoic acid and thyroid hormone regulate transcription of keratin genes.

Mechanisms of retinoic acid signalling and its roles in organ and limb development

Hair Cycle-Specific Immunolocalization of Retinoic Acid Synthesizing Enzymes Aldh1a2 and Aldh1a3 Indicate Complex Regulation

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