The Vitamin D Receptor Is Required for Mouse Hair Cycle Progression but Not for Maintenance of the Epidermal Stem Cell Compartment

March 2008 in “ The journal of investigative dermatology/Journal of investigative dermatology ”

Héctor G. Pálmer, Dolores Fernández Martínez, Geert Carmeliet, Fiona M. Watt

Studysummary This study suggests that while VDR is crucial for maintaining hair follicles in mice, their degeneration may be linked to impaired cell migration during hair growth phases rather than stem cell loss.

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The study concluded that the Vitamin D Receptor (VDR) was essential for hair cycle progression in mice but not for maintaining the epidermal stem cell compartment. VDR-null mice exhibited post-natal hair loss, hair follicle degeneration, and conversion into epidermal cysts due to impaired keratinocyte migration and lack of dermal papilla association. Despite a reduction in CD34/α6 double-positive keratinocytes, their clonal growth ability was not impaired, and label-retaining cells (LRCs) in VDR-null hair follicles responded to proliferative stimuli. The findings suggested that VDR played a role in regulating cell cycle genes and epidermal lineage selection.

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research Vitamin D Receptor Is Essential For Normal Keratinocyte Stem Cell Function

143 citations , May 2007 in “Proceedings of the National Academy of Sciences”

This study found that absence of the vitamin D receptor in keratinocytes impairs canonical Wnt signaling and leads to alopecia due to defects in keratinocyte stem cells.

research Development and Progression of Alopecia in the Vitamin D Receptor Null Mouse

81 citations , January 2006 in “Journal of cellular physiology”

This study found that the absence of the vitamin D receptor disrupts hair follicle structure during the first catagen in mice, linked to increased expression of the hairless gene.

research Physical And Functional Interaction Between The Vitamin D Receptor And Hairless Corepressor, Two Proteins Required For Hair Cycling

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.

research Manipulation of Stem Cell Proliferation and Lineage Commitment: Visualization of Label-Retaining Cells in Wholemounts of Mouse Epidermis

421 citations , September 2003 in “Development”

This study concluded that label-retaining cells in mouse epidermis differ in their sensitivity to proliferative stimuli, influencing their division and potential transdifferentiation without consistently depleting their population.

research Genetic Dissection of Retinoic Acid Function in Epidermis Physiology

9 citations , May 2002 in “PubMed”

This study demonstrated that mice lacking skin-specific RXRalpha expression developed hair follicle degeneration and alopecia, indicating the importance of RXRalpha/VDR heterodimers in maintaining hair follicle homeostasis.

research Atrichia Caused by Mutations in the Vitamin D Receptor Gene Is a Phenocopy of Generalized Atrichia Caused by Mutations in the Hairless Gene

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.

research Metabolic And Cellular Analysis Of Alopecia In Vitamin D Receptor Knockout Mice

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.

research Towards Defining the Pathogenesis of the Hairless Phenotype

86 citations , June 1998 in “Journal of Investigative Dermatology”

This study found that mutations in the hairless gene in mice disrupt hair follicle integrity during catagen, leading to baldness due to disintegrating epithelial structures and loss of normal dermal papilla.