title: Retinoid metabolism is altered in human and mouse cicatricial alopecia.
abstract: C57BL/6 mice develop dermatitis and scarring alopecia resembling human cicatricial alopecias (CAs), particularly the central centrifugal CA (CCCA) type. To evaluate the role of retinoids in CA, the expression of retinoid metabolism components were examined in these mice with mild, moderate, or severe CA compared with hair cycle-matched mice with no disease. Two feeding studies were conducted with dams fed either NIH 31 diet (study 1) or AIN93G diet (study 2). Adult mice were fed AIN93M diet with 4 (recommended), 28, or 56 IU vitamin A g(-1) diet. Feeding the AIN93M diet to adults increased CA frequency over NIH 31 fed mice. Increased follicular dystrophy was seen in study 1 and increased dermal scars in study 2 in mice fed the 28 IU diet. These results indicate that retinoid metabolism is altered in CA in C57BL/6J mice that require precise levels of dietary vitamin A. Human patients with CCCA, pseudopelade (end-stage scarring), and controls with no alopecia were also studied. Many retinoid metabolism proteins were increased in mild CCCA, but were undetectable in pseudopelade. Studies to determine whether these dietary alterations in retinoid metabolism seen in C57BL/6J mice are also involved in different types of human CA are needed.
authors.affiliation: Department of Nutrition, The Ohio State University, Columbus, Ohio, USA. everts.1@osu.edu
authors.forename: Helen B
authors.initials: HB
authors.lastname: Everts
authors.forename: Kathleen A
authors.initials: KA
authors.lastname: Silva
authors.forename: Shalise
authors.initials: S
authors.lastname: Montgomery
authors.forename: Liye
authors.initials: L
authors.lastname: Suo
authors.forename: Monica
authors.initials: M
authors.lastname: Menser
authors.forename: Amy S
authors.initials: AS
authors.lastname: Valet
authors.forename: Lloyd E
authors.initials: LE
authors.lastname: King
authors.forename: David E
authors.initials: DE
authors.lastname: Ong
authors.forename: John P
authors.initials: JP
authors.lastname: Sundberg
mesh_terms: D015096:3-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000367:Age Factors; D000505:Alopecia / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D000821:Animal Feed; D000818:Animals; D001706:Biopsy; D002921:Cicatrix / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D003872:Dermatitis / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D051379:Mice; D008810:Mice, Inbred C57BL; D018168:Receptors, Retinoic Acid / Q000378:metabolism; D000072482:Retinoic Acid Receptor alpha; D012176:Retinoids / Q000096:biosynthesis / Q000378:metabolism*; D012720:Severity of Illness Index; D015398:Signal Transduction / Q000502:physiology; D014801:Vitamin A / Q000493:pharmacokinetics*
chemical_list: C000607071:RARA protein, human; C000607072:Rara protein, mouse; D018168:Receptors, Retinoic Acid; D000072482:Retinoic Acid Receptor alpha; D012176:Retinoids; C082928:retinoic acid binding protein II, cellular; D014801:Vitamin A; D015096:3-Hydroxysteroid Dehydrogenases; C432414:DHRS9 protein, human