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

Everts, Helen B.; King, Lloyd E.; Sundberg, John P.; Ong, David E.

doi:10.1111/j.0022-202x.2004.23223.x

Cited by 29 publications

(22 citation statements)

References 32 publications

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“…ALDH1A3 catalyses the last step in retinoic acid synthesis. Previous reports have demonstrated specific expression in the hair follicle (Everts et al, 2004;Niederreither et al, 2002). Reduced levels of retinoic acid caused by the lack of ALDH1A3 may account for some effects in Foxn1::dnFgfr2-IIIb transgenic hair follicles.…”

Section: Discussionmentioning

confidence: 88%

FGF signals specifically regulate the structure of hair shaft medulla via IGF-binding protein 5

Schlake

2005

Development

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Reciprocal interactions between the dermal papilla and the hair matrix control proliferation and differentiation in the mature hair follicle. Analysis of expression suggests an important role for FGF7 and FGF10, as well as their cognate receptor FGFR2-IIIb, in these processes. Transgenic mice that express a soluble dominant-negative version of this receptor in differentiating hair keratinocytes were generated to interfere with endogenous FGF signalling. Transgenic mice develop abnormally thin but otherwise normal hairs, characterised by single columns of medulla cells in all hair types. All structural defects and the accompanying changes of global gene expression patterns are restricted to the hair medulla. Forced transgenic expression of IGF-binding protein 5, whose expression level is elevated upon suppression of FGFR2-IIIb-mediated signalling largely phenocopies the defect of dnFgfr2-IIIb-expressing hairs. Thus, the results identify Igfbp5-mediated FGFR2-IIIb signals as a key regulator of the genetic program that controls the structure of the hair shaft medulla.

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Section: Discussionmentioning

confidence: 88%

FGF signals specifically regulate the structure of hair shaft medulla via IGF-binding protein 5

Schlake

2005

Development

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“…Airway epithelial cells express Aldh1a1 and might also constitute a source of GM-CSF. 31,35,36 In the skin, the RALDH2 and RALDH3 enzymes are highly expressed by hair follicles, 37,38 whereas GM-CSF is produced by keratinocytes and dermal fibroblasts. 39,40 Therefore, these recurrent features may explain the presence of ALDH ϩ DCs in the small intestine, lungs, and skin and point to the existence of cellular niches capable of inducing ALDH activity in DCs.…”

Section: Discussionmentioning

confidence: 99%

Skin-draining lymph nodes contain dermis-derived CD103− dendritic cells that constitutively produce retinoic acid and induce Foxp3+ regulatory T cells

Guilliams

Crozat

Henri

et al. 2010

Blood

286

293

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Small intestinal CD103 ؉ dendritic cells (DCs) have the selective ability to promote de novo generation of regulatory T cells via the production of retinoic acid (RA). Considering that aldehyde dehydrogenase (ALDH) activity controls the production of RA, we used a flow cytometrybased assay to measure ALDH activity at the single-cell level and to perform a comprehensive analysis of the RA-producing DC populations present in lymphoid and nonlymphoid mouse tissues. RA-producing DCs were primarily of the tissue-derived, migratory DC subtype and can be readily found in the skin and in the lungs as well as in their corresponding draining lymph nodes. The RA-producing skin-derived DCs were capable of triggering the generation of regulatory T cells, a finding demonstrating that the presence of RA-producing, tolerogenic DCs is not restricted to the intestinal tract as previously thought. Unexpectedly, the production of RA by skin DCs was restricted to CD103 ؊ DCs, indicating that CD103 expression does not constitute a "universal" marker for RA-producing mouse DCs. Finally, Toll-like receptor (TLR) triggering or the presence of a commensal microflora was not essential for the induction of ALDH activity in the discrete ALDH ؉ DC subsets that characterize tissues constituting environmental interfaces. (Blood. 2010;115: 1958-1968 IntroductionThe vitamin A metabolite retinoic acid (RA) is a lipophilic molecule that controls the activity of a constellation of genes via binding to nuclear receptors. 1 Vitamin A is derived from the diet, and the liver constitutes a large reservoir of vitamin A in the form of retinyl esters. Retinyl esters are hydrolyzed to retinol and released into the blood. Once retinol enters cells expressing appropriate enzymes, it is converted successively into retinal and RA. The first step of the conversion is catalyzed by alcohol dehydrogenases and by microsomal retinol dehydrogenases that are expressed by most cells, including dendritic cells (DCs). The second step consists of the oxidation of retinal into RA and is catalyzed by 3 aldehyde dehydrogenases (ALDHs), known as RALDH1, 2, and 3 and encoded by the Aldh1a1, -2, and -3 genes, respectively. RALDH expression is limited to certain cell types and, despite the widespread availability of retinol, only cells expressing one of the RALDHs can oxidize retinaldehyde to RA.Conventional DCs (cDCs) and plasmacytoid DCs (pDCs) reside throughout their life cycle in secondary lymphoid organs and are denoted as lymphoid tissue-resident DCs to distinguish them from tissue-derived, migratory DCs (mDCs). 2 cDCs express intermediate levels of major histocompatibility complex (MHC) class II molecules and high levels of CD11c (MHCII inter CD11c high ), whereas mDCs express high levels of MHC class II molecules and intermediate to high levels of CD11c (MHCII high CD11c inter to high ). Recently, DCs that are located in gut-associated lymphoid tissue (GALT) and express Aldh1a2 have gained considerable attention because of their ability to produce RA. On migration to me...

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“…This finding needs to be further examined in patients with AA, as most humans with AA have fewer hair follicles in anagen. 24 We also reported that RA synthesis and signaling protein localization within the hair follicle was altered during the hair cycle, 25, 26 although few studies have examined how the hair cycle is regulated by vitamin A.…”

Section: Introductionmentioning

confidence: 99%

Dietary vitamin A regulates wingless-related MMTV integration site signaling to alter the hair cycle

Suo

Sundberg

Everts

2014

Exp Biol Med (Maywood)

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Alopecia areata is an autoimmune hair loss disease caused by a cell mediated immune attack of the lower portion of the cycling hair follicle. Feeding mice 3–7 times the recommended level of dietary vitamin A accelerated the progression of alopecia areata in the graft-induced C3H/HeJ mouse model of alopecia areata. In this study we also found that dietary vitamin A, in a dose dependent manner, activated the hair follicle stem cells to induce the development and growth phase of the hair cycle (anagen), which may have made the hair follicle more susceptible to autoimmune attack. Our purpose here is to determine the mechanism by which dietary vitamin A regulates the hair cycle. We found that vitamin A in a dose dependent manner increased nuclear localized beta-catenin (CTNNB1; a marker of canonical WNT signaling) and levels of WNT7A (wingless-related MMTV integration site 7A) within the hair follicle bulge in these C3H/HeJ mice. These findings suggest that feeding mice high levels of dietary vitamin A increases WNT signaling to activate hair follicle stem cells.

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

Cited by 29 publications

References 32 publications

FGF signals specifically regulate the structure of hair shaft medulla via IGF-binding protein 5

FGF signals specifically regulate the structure of hair shaft medulla via IGF-binding protein 5

Skin-draining lymph nodes contain dermis-derived CD103− dendritic cells that constitutively produce retinoic acid and induce Foxp3+ regulatory T cells

Dietary vitamin A regulates wingless-related MMTV integration site signaling to alter the hair cycle

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