scholarly journals Vitamin A Metabolism During Refractory Telogen

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 109-109
Author(s):  
Damla Hovland ◽  
Liye Suo ◽  
Natalia Kedishvili ◽  
John Sundberg ◽  
Helen Everts
Keyword(s):  
Vitamin A ◽  
Hair Follicles ◽  
Dietary Vitamin ◽  
Hair Cycle ◽  
Retinol Dehydrogenase ◽  
Vitamin A Metabolism ◽  
Funding Sources ◽  
Morphogenetic Protein ◽  
Bmp4 Expression ◽  
Complete Set

Abstract Objectives Hair follicles cycle through periods of growth (anagen), regression (catagen) and rest (telogen). Telogen is further divided into refractory and competent telogen based on the expression of bone morphogenetic protein 4 (BMP4). Previously, the expression of a complete set of proteins involved in retinoic acid (RA) synthesis and signaling localized to the hair follicle and changed throughout the hair cycle. In addition, excess dietary vitamin A arrested the hair cycle in telogen; while retinol dehydrogenases short-chain dehydrogenase/reductase family 16C members 5 and 6 (Sdr16c5−/−/Sdr16c6−/−) double null mice had an accelerated the hair cycle. The purpose of this study was to further define these changes in the hair cycle. Methods The localization of RA synthesis proteins SDR16C5, retinol dehydrogenase 10 (RDH10), retinal dehydrogenase 2 (ALDH1A2), cellular RA binding protein 2 (CRABP2), RA degradation enzyme cytochrome p450 26B1 (CYP26B1), and BMP4 was examined in telogen hair follicles in female C57BL/6 J mice by immunohistochemistry. Immunohistochemistry with an antibody against BMP4 was also used to mark refractory telogen in the previous dietary vitamin A study. Results All proteins localized to BMP4 positive refractory telogen hair follicles. SDR16C5 and ALDH1A2 were also seen in BMP4 negative competent telogen hair follicles, but at a lower level. RDH10 was expressed in both BMP4 negative and positive hair follicles at similar levels. BMP4 expression was also used to distinguish refractory from competent telogen in C57BL/6 J mice fed different levels of vitamin A. Both low and excess dietary vitamin A resulted a greater percentage of hair follicles in refractory telogen in different studies. Conclusions In conclusion, RA synthesis and signaling may be stronger in refractory telogen and contribute to the inhibition of the hair cycle. Funding Sources NIH/NIAMS, Internal funding.

scholarly journals Dietary Vitamin A Impacts Refractory Telogen

2021 ◽  
Vol 9 ◽  
Author(s):  
Liye Suo ◽  
Christine VanBuren ◽  
Eylul Damla Hovland ◽  
Natalia Y. Kedishvili ◽  
John P. Sundberg ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Vitamin A ◽  
Hair Follicle ◽  
Integration Site ◽  
Acid Synthesis ◽  
Hair Follicles ◽  
Dietary Vitamin ◽  
Dependent Manner ◽  
Hair Cycle ◽  
Retinyl Esters

Hair follicles cycle through periods of growth (anagen), regression (catagen), rest (telogen), and release (exogen). Telogen is further divided into refractory and competent telogen based on expression of bone morphogenetic protein 4 (BMP4) and wingless-related MMTV integration site 7A (WNT7A). During refractory telogen hair follicle stem cells (HFSC) are inhibited. Retinoic acid synthesis proteins localized to the hair follicle and this localization pattern changed throughout the hair cycle. In addition, excess retinyl esters arrested hair follicles in telogen. The purpose of this study was to further define these hair cycle changes. BMP4 and WNT7A expression was also used to distinguish refractory from competent telogen in C57BL/6J mice fed different levels of retinyl esters from two previous studies. These two studies produced opposite results; and differed in the amount of retinyl esters the dams consumed and the age of the mice when the different diet began. There were a greater percentage of hair follicles in refractory telogen both when mice were bred on an unpurified diet containing copious levels of retinyl esters (study 1) and consumed excess levels of retinyl esters starting at 12 weeks of age, as well as when mice were bred on a purified diet containing adequate levels of retinyl esters (study 2) and remained on this diet at 6 weeks of age. WNT7A expression was consistent with these results. Next, the localization of vitamin A metabolism proteins in the two stages of telogen was examined. Keratin 6 (KRT6) and cellular retinoic acid binding protein 2 (CRABP2) localized almost exclusively to refractory telogen hair follicles in study 1. However, KRT6 and CRABP2 localized to both competent and refractory telogen hair follicles in mice fed adequate and high levels of retinyl esters in study 2. In mice bred and fed an unpurified diet retinol dehydrogenase SDR16C5, retinal dehydrogenase 2 (ALDH1A2), and cytochrome p450 26B1 (CYP26B1), enzymes and proteins involved in RA metabolism, localized to BMP4 positive refractory telogen hair follicles. This suggests that vitamin A may contribute to the inhibition of HFSC during refractory telogen in a dose dependent manner.

scholarly journals The interaction of selenoprotein F (SELENOF) with retinol dehydrogenase 11 (RDH11) implied a role of SELENOF in vitamin A metabolism

2018 ◽  
Vol 15 (1) ◽  
Author(s):  
Jing Tian ◽  
Jiapan Liu ◽  
Jieqiong Li ◽  
Jingxin Zheng ◽  
Lifang Chen ◽  
...  
Keyword(s):  
Vitamin A ◽  
Retinol Dehydrogenase ◽  
Vitamin A Metabolism

scholarly journals 244.Interaction between bone morphogenetic protein 4 and retinoid signalling in mouse spermatogenesis

2004 ◽  
Vol 16 (9) ◽  
pp. 244
Author(s):  
R. M. Baleato ◽  
R. J. Aitken ◽  
S. D. Roman
Keyword(s):  
Gene Expression ◽  
Vitamin A ◽  
Bone Morphogenetic Protein ◽  
Germ Cells ◽  
Molecular Mechanisms ◽  
Vitamin A Deficiency ◽  
Morphogenetic Protein ◽  
Bmp4 Expression ◽  
High Doses

Vitamin A (retinol, or ROL) is also essential for normal spermatogenesis in the rat and mouse. Vitamin A-deficient (VAD) rodents suffer various disorders including blindness and male infertility. The molecular mechanisms leading to infertility in vitamin A deficient rodents have never been fully elucidated. Following prolonged vitamin A withdrawal the only germ cells remaining in the VAD rodent testis are stem cell spermatogonia, type A1 spermatogonia, and a few preleptotene spermatocytes. Supplementing the diet of these animals with retinoic acid (RA) alleviates all symptoms of vitamin A deficiency, with the exception of sight and spermatogenesis. It is not until VAD animals are re-administered ROL through the diet, or RA is injected in repeated high doses directly into the testis, that normal spermatogenic function is restored. Here we report an interaction, in germ cells, between the Bone Morphogenetic Protein (BMP) 4 and retinoid signalling pathways that may help explain the molecular mechanics of vitamin A deficiency. We localised BMP4 gene expression to adult germ cells, in particular spermatogonia, at both the mRNA and protein level. We generated VAD mice and found that in the absence of retinoids in vivo, bmp4 gene expression was significantly upregulated in the testis. We also observed that the expression of bmp4 is downregulated by retinoid treatment in germ cells isolated from vitamin A sufficient mice. Expression of bmp4 mRNA in isolated spermatogonia was more sensitive to ROL rather than RA. Our results may reflect a direct requirement for ROL by germ cells for the resumption of spermatogenesis in VAD animals that involves the regulation of BMP4 expression. Furthermore our observations suggest that retinoid signalling in germ cells is different to that observed in somatic cells, and may provide insights into the role of retinoids in spermatogenesis.

scholarly journals Retinoids in Cutaneous Squamous Cell Carcinoma

Nutrients ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 153
Author(s):  
Helen B. Everts ◽  
Eleonore-Nausica Akuailou
Keyword(s):  
Squamous Cell Carcinoma ◽  
Vitamin A ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Animal Studies ◽  
Vitamin A Deficiency ◽  
Cutaneous Squamous Cell Carcinoma ◽  
Dietary Vitamin ◽  
Vitamin A Metabolism ◽  
Ultraviolet Light B

Animal studies as early as the 1920s suggested that vitamin A deficiency leads to squamous cell metaplasia in numerous epithelial tissues including the skin. However, humans usually die from vitamin A deficiency before cancers have time to develop. A recent long-term cohort study found that high dietary vitamin A reduced the risk of cutaneous squamous cell carcinoma (cSCC). cSCC is a form of nonmelanoma skin cancer that primarily occurs from excess exposure to ultraviolet light B (UVB). These cancers are expensive to treat and can lead to metastasis and death. Oral synthetic retinoids prevent the reoccurrence of cSCC, but side effects limit their use in chemoprevention. Several proteins involved in vitamin A metabolism and signaling are altered in cSCC, which may lead to retinoid resistance. The expression of vitamin A metabolism proteins may also have prognostic value. This article reviews what is known about natural and synthetic retinoids and their metabolism in cSCC.

Vitamin A Metabolism in Infection

1955 ◽  
Vol 57 (2) ◽  
pp. 277-286 ◽  
Author(s):  
B. M. Kagan ◽  
Elizabeth Kaiser
Keyword(s):  
Vitamin A ◽  
Vitamin A Metabolism

scholarly journals Dietary vitamin A supplementation in rats: suppression of leptin and induction of UCP1 mRNA

1999 ◽  
Vol 40 (5) ◽  
pp. 824-829 ◽  
Author(s):  
Monica V. Kumar ◽  
Gregory D. Sunvold ◽  
Philip J. Scarpace
Keyword(s):  
Vitamin A ◽  
Dietary Vitamin ◽  
Vitamin A Supplementation

scholarly journals The complexity of producing and interpreting dietary vitamin A statistics

2021 ◽  
pp. 103926
Author(s):  
Ana Moltedo ◽  
Cristina Álvarez-Sánchez ◽  
Fernanda Grande ◽  
Ruth Charrondiere
Keyword(s):  
Vitamin A ◽  
Dietary Vitamin

scholarly journals Localisation and regulation of cholesterol transporters in the human hair follicle: mapping changes across the hair cycle

2021 ◽  
Author(s):  
Megan A. Palmer ◽  
Eleanor Smart ◽  
Iain S. Haslam
Keyword(s):  
Hair Follicle ◽  
Human Hair ◽  
Vital Role ◽  
Transport Proteins ◽  
Hair Follicles ◽  
Regulatory Control ◽  
Cholesterol Transport ◽  
Hair Cycle ◽  
Human Hair Follicle

AbstractCholesterol has long been suspected of influencing hair biology, with dysregulated homeostasis implicated in several disorders of hair growth and cycling. Cholesterol transport proteins play a vital role in the control of cellular cholesterol levels and compartmentalisation. This research aimed to determine the cellular localisation, transport capability and regulatory control of cholesterol transport proteins across the hair cycle. Immunofluorescence microscopy in human hair follicle sections revealed differential expression of ATP-binding cassette (ABC) transporters across the hair cycle. Cholesterol transporter expression (ABCA1, ABCG1, ABCA5 and SCARB1) reduced as hair follicles transitioned from growth to regression. Staining for free cholesterol (filipin) revealed prominent cholesterol striations within the basement membrane of the hair bulb. Liver X receptor agonism demonstrated active regulation of ABCA1 and ABCG1, but not ABCA5 or SCARB1 in human hair follicles and primary keratinocytes. These results demonstrate the capacity of human hair follicles for cholesterol transport and trafficking. Future studies examining the role of cholesterol transport across the hair cycle may shed light on the role of lipid homeostasis in human hair disorders.

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