TY - JOUR
T1 - The Transient Role for Calcium and Vitamin D during the Developmental Hair Follicle Cycle
AU - Mady, Leila J.
AU - Ajibade, Dare V.
AU - Hsaio, Connie
AU - Teichert, Arnaud
AU - Fong, Chak
AU - Wang, Yongmei
AU - Christakos, Sylvia
AU - Bikle, Daniel D.
N1 - Funding Information:
Support was provided by NIH Grant DK38961-22 (SC), NIH Grant AR050023 (DB), VA Merit Review grant (DB), DOD Grant CA110338 (DB), and a United Negro College Fund Merck Graduate Student Research Dissertation Fellowship (DVA). We acknowledge helpful discussions with and assistance of Dr. Puneet Dhawan and Dr. Peter Elias in certain aspects of this investigation. The Calbindin-D9k KO mice were provided to Dr. Christakos by Drs. EB Jeung and GT Oh.
PY - 2016/7/1
Y1 - 2016/7/1
N2 - The role for 1,25-dihydroxyvitamin D3 and/or calcium in hair follicle cycling is not clear despite their impact on keratinocyte differentiation. We found that calbindin-D9k null (knockout) pups generated from calbindin-D9k knockout females fed a vitamin D-deficient, low-calcium (0.47%) diet develop transient alopecia. The pups appear phenotypically normal until 13 days of age, after which the hair progressively sheds in a caudocephalic direction, resulting in truncal alopecia totalis by 20–23 days, with spontaneous recovery by 28 days. Histological studies showed markedly dystrophic hair follicles, loss of hair shafts with increased apoptosis, and hyperplastic epidermis during this time. Ha1 expression is lost during catagen in all mice but recovers more slowly in the knockout pups on the vitamin D-deficient, low-calcium diet. Keratin 1 expression is reduced throughout days 19–28. The expressions of involucrin, loricrin, and cathepsin L is initially increased by day 19 but subsequently falls below those of controls by day 23, as does that of desmoglein 3. Feeding the mothers a high-vitamin D/high-calcium (2%)/lactose (20%) diet lessens the phenotype, and knockout pups fostered to mothers fed a normal diet do not develop alopecia. Our results show that in calbindin-D9k knockout pups, a maternal vitamin D-deficient/low-calcium diet leads to transient noncicatricial alopecia.
AB - The role for 1,25-dihydroxyvitamin D3 and/or calcium in hair follicle cycling is not clear despite their impact on keratinocyte differentiation. We found that calbindin-D9k null (knockout) pups generated from calbindin-D9k knockout females fed a vitamin D-deficient, low-calcium (0.47%) diet develop transient alopecia. The pups appear phenotypically normal until 13 days of age, after which the hair progressively sheds in a caudocephalic direction, resulting in truncal alopecia totalis by 20–23 days, with spontaneous recovery by 28 days. Histological studies showed markedly dystrophic hair follicles, loss of hair shafts with increased apoptosis, and hyperplastic epidermis during this time. Ha1 expression is lost during catagen in all mice but recovers more slowly in the knockout pups on the vitamin D-deficient, low-calcium diet. Keratin 1 expression is reduced throughout days 19–28. The expressions of involucrin, loricrin, and cathepsin L is initially increased by day 19 but subsequently falls below those of controls by day 23, as does that of desmoglein 3. Feeding the mothers a high-vitamin D/high-calcium (2%)/lactose (20%) diet lessens the phenotype, and knockout pups fostered to mothers fed a normal diet do not develop alopecia. Our results show that in calbindin-D9k knockout pups, a maternal vitamin D-deficient/low-calcium diet leads to transient noncicatricial alopecia.
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U2 - 10.1016/j.jid.2016.02.813
DO - 10.1016/j.jid.2016.02.813
M3 - Article
C2 - 26994969
AN - SCOPUS:84992476847
VL - 136
SP - 1337
EP - 1345
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
SN - 0022-202X
IS - 7
ER -