New Aspects of Vitamin D Metabolism and Action: Addressing the Skin as Source and Target

This study found that the vitamin D receptor is essential for the self-renewal, migration, and differentiation of epidermal stem cells during skin wound healing in mice.

This study found that individuals with alopecia areata had significantly lower serum vitamin D levels and a higher prevalence of vitamin D deficiency compared to people without the condition.

This study found that vitamin D deficiency in patients with alopecia areata was associated with greater disease severity and longer duration, but not with disease pattern or vitamin D receptor expression.

In this study, the researchers found that vitamin D and calcium signaling in keratinocytes are essential for normal skin regeneration after wounding, with deficiencies significantly delaying wound closure and re-epithelialization in mice.

This study found that calbindin-D9k knockout mice on a maternal vitamin D-deficient and low-calcium diet developed transient alopecia, but a high-vitamin D and calcium diet in mothers reduced this effect.

This study found that in a mouse model with hereditary 1,25-dihydroxyvitamin D resistant rickets, a mutant vitamin D receptor lacking hormone-binding ability could restore normal hair cycling and affect parathyroid hormone regulation.

This study highlights the complex role of the vitamin D receptor in skin processes, where its disruption, along with calcium and co-regulator imbalances, could contribute to skin cancer development by altering skin differentiation and hair follicle cycling.

This study found that the absence of unliganded vitamin D receptor significantly impairs cWnt and hedgehog signaling pathways necessary for hair cycle initiation in VDR-null mice.

This study created a humanized mouse model of hereditary vitamin D-resistant rickets that lacks alopecia, indicating the mutant receptor's potential to explore the syndrome's characteristics beyond vitamin D binding.

This review discusses various stem cell compartments in adult murine and human epidermis, examining their expressed markers and characterization assays, and reports no new experimental results.

This abstract reviews hereditary vitamin D-resistant rickets, a rare genetic condition causing severe early childhood rickets, and reports no new results; effective treatment typically requires high doses of calcium to address hypocalcemia and secondary hyperparathyroidism.

This study found that 1,25-dihydroxyvitamin D3/VDR inhibits β-catenin's role in keratinocyte proliferation but enhances its role in hair follicle differentiation.

This study found that the absence of vitamin D receptor signaling in mice impairs the inflammatory response to skin injury, particularly affecting macrophage recruitment and granulation tissue formation.

This study found that hair follicle stem cells initially contribute to wound re-epithelialization, but long-lasting epidermal cells are primarily derived from a stem cell population in the isthmus portion of hair follicles.

This study reported that deleting the MED1 subunit from the MED complex in keratinocytes resulted in disrupted hair differentiation and cycling, leading to hair loss in mice.

This study found that while calcium can substitute for the Vitamin D receptor in maintaining epidermal keratinocyte differentiation, it cannot compensate for hair follicle dysfunction caused by the absence of the receptor.

This review examines the functions of vitamin D and its receptor in skin and explores how these are regulated, reporting no new clinical results.

Lack of vitamin D receptor increases skin tumor risk by boosting hedgehog signaling.

This review discusses the regulation and function of vitamin D and its receptor in skin cells, highlighting their roles in processes such as proliferation inhibition, differentiation, and innate immunity, but reports no new results.

This study discovered a novel interaction between the vitamin D receptor and LEF1, essential for normal Wnt signaling in keratinocytes, which is crucial for regular hair cycling.

This study found that mice lacking the Vitamin D receptor showed disrupted hair follicle cycling, which was partially restored with hedgehog signaling pathway activation, suggesting a role for this pathway in follicle regulation independent of vitamin D.

This study concluded that the hairless protein interacts with the vitamin D receptor to repress transcription crucial for hair cycling, employing multiple protein interfaces and modulating chromatin structure.

This review summarizes fundamental concepts and recent advancements in hair follicle biology, including insights from mouse models into broader molecular and cellular processes relevant to regeneration and development.

This study found that mice lacking the vitamin D receptor (VDR) developed skin tumors more rapidly than those with normal VDR activity, regardless of 1,25-dihydroxyvitamin D(3) presence.

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.

This study observed that the vitamin D receptor is crucial for hair follicle formation and altering tumor development in the Wnt signaling pathway, suggesting therapeutic potential for vitamin D analogues in related tumors.

This review examines beta-catenin's role in stem cell renewal, lineage selection, and tumor formation in the epidermis and reports no new experimental findings.

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.

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.

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.

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.

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.

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.

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.

This study identified the presence of the enzyme 1 alpha-hydroxylase in various extrarenal tissues, suggesting its potential role in modulating vitamin D function in peripheral tissues.

In this study, the researchers found that alopecia in VDR null mice is likely due to issues with hair cycle initiation rather than defects in keratinocyte proliferation or differentiation.

This study found that basal cell carcinomas show strong expression of vitamin D receptors at both mRNA and protein levels, suggesting a potential role in tumor growth regulation.

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.

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.

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.

This study found that alopecia in four children was linked to severe calcitriol-resistant rickets, suggesting this condition should be considered among inherited hair growth disorders.

Vitamin D3 affects cell differentiation in specific skin areas.