95 citations
,
July 2006 in “British Journal of Dermatology” This study observed that vitamin D receptor expression in certain hair follicle cells varies throughout the murine hair cycle, suggesting a potential role for 1,25-dihydroxyvitamin D3 in hair follicle biology.
78 citations
,
November 2005 in “Endocrinology” This study found that Hairless (Hr) acts as a corepressor of the vitamin D receptor (VDR) in human keratinocytes, blocking the action of vitamin D on keratinocyte differentiation.
144 citations
,
December 2004 in “Molecular Endocrinology” This study found that the effects of the vitamin D receptor on hair follicle cycling in mice are independent of its ability to bind a hormone, with specific domain mutations influencing hair regrowth outcomes.
140 citations
,
April 2004 in “The journal of investigative dermatology/Journal of investigative dermatology” This study found that mice lacking the 1αOHase enzyme, which is responsible for producing a key vitamin D metabolite, showed impaired epidermal differentiation and delayed recovery of skin barrier function after disruption.
215 citations
,
September 2003 in “Journal of Biological Chemistry” This study found that the hairless gene product (Hr) suppresses VDR-mediated gene activation by directly interacting with the vitamin D receptor, potentially affecting hair follicle function.
57 citations
,
April 2002 in “The journal of investigative dermatology/Journal of investigative dermatology” This study found that the vitamin D receptor is crucial for initiating the postnatal hair follicular cycle in mice, preventing alopecia associated with its inactivation.
854 citations
,
February 2002 in “The journal of investigative dermatology/Journal of investigative dermatology” This review summarizes recent advances in understanding the molecular mechanisms of hair follicle formation and discusses potential future clinical applications for treating hair loss and skin tumors, but it reports no new clinical results.
180 citations
,
January 2002 in “The journal of investigative dermatology/Journal of investigative dermatology” This study observed that vitamin D receptor knockout mice exhibit impaired epidermal differentiation and progressive hair loss, suggesting the importance of the vitamin D receptor in normal skin and hair follicle development.
115 citations
,
December 2001 in “Endocrinology” This study found that restoring vitamin D receptor expression specifically in the keratinocytes of VDR null mice prevented alopecia and enhanced hair follicle response during anagen initiation.
139 citations
,
September 2001 in “The journal of investigative dermatology/Journal of investigative dermatology” This case report describes a patient with mutations in both alleles of the vitamin D receptor who exhibited hair loss clinically indistinguishable from generalized atrichia with papules, suggesting a potential genetic pathway shared with the hairless gene.
54 citations
,
May 2001 in “Journal of Investigative Dermatology” This study suggests that increased putrescine levels may disrupt normal hair follicle development in transgenic mice, leading to hair loss and altered skin structure, yet these mice appear more resistant to skin tumorigenesis.
137 citations
,
April 2001 in “Journal of Clinical Investigation” This study found that alopecia in VDR-null mice persists despite undetectable vitamin D levels, indicating a defect in epithelial-mesenchymal communication due to the absence of ligand-independent receptor function.
303 citations
,
October 2000 in “Nature” This study found that RXRα plays a critical role in hair cycling and keratinocyte functions in mice, likely through its interaction with VDR in epidermal cells.
29 citations
,
June 2000 in “Endocrinology” This study suggests that alopecia in vitamin D receptor null mice is due to impaired initiation of the hair cycle rather than defects in keratinocyte proliferation or differentiation.
20 citations
,
April 2000 in “Experimental dermatology” This study observed that overexpression of the enzyme ODC in transgenic mice caused hair loss and skin changes similar to human papular atrichia, suggesting that ODC might be involved in a critical hair follicle function pathway.
166 citations
,
July 1999 in “American Journal Of Pathology” This study found that the loss of a functional hr gene in mice leads to premature and abnormal hair follicle regression, disrupting normal hair cycling and architecture.
519 citations
,
October 1998 in “Endocrinology” The study found that normalizing mineral ion levels in vitamin D receptor-ablated mice prevented hyperparathyroidism and bone disorders but did not address hair loss, indicating the VDR's role in hair growth.
126 citations
,
October 1998 in “Experimental Dermatology” This review provides an overview of the hairless gene in mice and humans, discussing its structure, expression, and implications for understanding skin physiology and human disorders related to gene disruption, but it reports no new empirical findings.
412 citations
,
January 1998 in “Science” This study identified a missense mutation in the human hairless gene associated with a rare form of recessively inherited alopecia universalis, pinpointed on chromosome 8p12.
71 citations
,
May 1996 in “Journal of Investigative Dermatology” This study found that overexpression of a mutated ornithine decarboxylase transgene in mice led to complete hair loss, which could be prevented or reversed with an ODC inhibitor.
66 citations
,
August 1990 in “Journal of Investigative Dermatology” Epithelial cell growth in rat hair follicles needs contact with mesenchymal cells through the extracellular matrix.
100 citations
,
October 1986 in “Clinical Endocrinology” This study found that alopecia in hereditary resistance to 1,25(OH)2D may indicate a more severe form of the condition, associated with earlier diagnosis and different responses to calciferol therapy.
11 citations
,
May 1985 in “Archives of Dermatology” This study found that calcitriol-resistant rickets is associated with alopecia in children and should be considered in the differential diagnosis of hair loss.