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. 2012 Jan;1821(1):222-9.
doi: 10.1016/j.bbalip.2011.08.017. Epub 2011 Sep 3.

Endogenous Retinoids in the Hair Follicle and Sebaceous Gland

Free PMC article

Endogenous Retinoids in the Hair Follicle and Sebaceous Gland

Helen B Everts. Biochim Biophys Acta. .
Free PMC article


Vitamin A and its derivatives (retinoids) are critically important in the development and maintenance of multiple epithelial tissues, including skin, hair, and sebaceous glands, as shown by the detrimental effects of either vitamin A deficiency or toxicity. Thus, precise levels of retinoic acid (RA, active metabolite) are needed. These precise levels of RA are achieved by regulating several steps in the conversion of dietary vitamin A (retinol) to RA and RA catabolism. This review discusses the localization of RA synthesis to specific sites within the hair follicle and sebaceous gland, including their stem cells, during both homeostasis and disease states. It also discusses what is known about the specific roles of RA within the hair follicle and sebaceous gland. This article is part of a Special Issue entitled: Retinoid and Lipid Metabolism.


Figure 1
Figure 1. Cellular retinol metabolism in the skin
Once inside the cell, retinol is either stored as retinyl esters, or oxidized to retinoic acid (RA). Several families of enzymes and binding proteins are involved in this process.
Figure 2
Figure 2. The hair follicle
The hair follicle is illustrated with structures labeled as they change during the hair cycle.
Figure 3
Figure 3. Retinoic acid synthesis in the hair follicle
Telogen (a) and anagen (b) hair follicles are color coded with retinoic acid synthesis components: DHRS9 plus RARs (yellow), DHRS9 alone (pink), RARs alone (purple), CRABP2 (blue), CRBP (green), ALDH1A1, 2, or 3 (orange), a complete system with DHRS9, ALDH1A1, 2, or 3, CRABP2, and RARa, b,or g (red). Stem cell locations are marked in relation to this localization pattern of RA synthesis components. (c) RA synthesis as determined by immunohistochemistry with an antibody against beta-galactosidase in RA reporter mice (Tg(RARE-Hspa1b/lacz)12Jrt/J). Modified from Everts et al [24].

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