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Related Experiment Video

Updated: Jul 14, 2026

Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin

Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin

Published on: July 14, 2017

Vitamin D receptor is essential for normal keratinocyte stem cell function.

Luisella Cianferotti¹, Megan Cox, Kristi Skorija

¹Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA

Proceedings of the National Academy of Sciences of the United States of America

|May 23, 2007

Summary

The vitamin D receptor (VDR) plays a ligand-independent role in hair follicle regeneration. Its absence impairs Wnt signaling in keratinocytes, leading to alopecia and reduced stem cell function.

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Last Updated: Jul 14, 2026

Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin

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Published on: July 14, 2017

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Cultivating a Three-dimensional Reconstructed Human Epidermis at a Large Scale

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Published on: May 28, 2021

Area of Science:

Dermatology
Molecular Biology
Genetics

Background:

The vitamin D receptor (VDR) is crucial for mineral ion homeostasis.
VDR mutations in humans and mice cause alopecia, indicating a role beyond mineral balance.
The VDR's function in preventing alopecia is independent of its ligand-binding activity.

Purpose of the Study:

To investigate the ligand-independent role of the VDR in hair follicle stem cell function.
To elucidate the mechanism by which VDR absence leads to alopecia.
To explore the VDR's involvement in canonical Wnt signaling pathways within keratinocytes.

Main Methods:

Analysis of VDR-null mice models to study alopecia.
In vivo and in vitro assays assessing keratinocyte stem cell regeneration and colony formation.
Transient gene expression assays to evaluate the impact on beta-catenin and Lef1 transcriptional activity.

Main Results:

VDR absence does not prevent stem cell niche formation but impairs hair follicle regeneration.
VDR-null mice exhibit decreased keratinocyte stem cells and increased sebaceous activity.
The cooperative transcriptional effects of beta-catenin and Lef1 are abolished in VDR-null keratinocytes, indicating impaired Wnt signaling.

Conclusions:

The unliganded VDR is essential for maintaining canonical Wnt signaling in keratinocytes.
Impaired Wnt signaling due to VDR absence leads to alopecia through defective keratinocyte stem cell function.
This study reveals a novel, ligand-independent role for VDR in hair follicle biology.