Abstract

In this short review, I introduce an integrated vision of human hair follicle behavior and describe opposing influences that control hair follicle homeostasis, from morphogenesis to hair cycling. The interdependence and complementary roles of these influences allow us to propose that the hair follicle is a true paradigm of a “Yin Yang” type, that is a cold/slow-hot/fast duality. Moreover, a new promising field is emerging, suggesting that glycans are key elements of hair follicle growth control.

Highlights

  • The hair follicle is a true paradigm of mesenchymal-epithelial interaction

  • Its bi-stability and the intense remodeling processes that it provokes rely on the permanent dialog between opposing and complementary influences, impacting all follicle compartments

  • One can understand that an optimal way to describe the complex equilibrium which controls hair follicle homeostasis is the concept of “Yin Yang”

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Summary

Introduction

The hair follicle is a true paradigm of mesenchymal-epithelial interaction. From early morphogenesis to a fully formed organ, the hair follicle life-cycle is controlled by a dialog between mesenchymal and epithelial compartments[1]. With respect to key regulators of hair follicle growth and cycling, syndecans modulate Wnt signaling cascades[57], the glycosaminoglycan chains of proteoglycans shape Hedgehog gradients and signal transduction[58], and O-linked glycosylation controls Notch[1] interaction with its cognate Delta-like 4 receptor[59]. A small leucine-rich proteoglycan, directly modulates TGF-β, epidermal growth factor (EGF), IGF-1 and hepatocyte growth factor (HGF) signaling, all known actors of hair follicle cycling[60], and appears to act as an anagen inducer[61]. These recent results designate glycans as long time ignored key players in hair growth control. From a clinical point of view, alterations of glycosaminoglycan degradation provoke mucopolysaccharidoses and abnormalities in hair morphology[68], which can be reversed by appropriate enzyme replacement therapy[69]

Conclusion
Turing A
24. Imamura T
PubMed Abstract
47. Couchman JR
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