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First published online 8 April 2008
doi: 10.1242/jcs.018689

Journal of Cell Science 121, 1435-1443 (2008)
Published by The Company of Biologists 2008
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Research Article

Control of thrombin signaling through PI3K is a mechanism underlying plasticity between hair follicle dermal sheath and papilla cells

Anne-Catherine Feutz1,*, Yann Barrandon2 and Denis Monard1,{ddagger}

1 Friedrich Miescher Institute for Biomedical Research, CH-4058, Basel, Switzerland
2 Laboratory of Stem Cell Dynamics, Ecole Polytechnique Fédérale de Lausanne and Lausanne University Hospital, Station 15, CH-1015 Lausanne, Switzerland

{ddagger} Author for correspondence (e-mail: monard{at}fmi.ch)

Accepted 26 January 2008

In hair follicles, dermal papilla (DP) and dermal sheath (DS) cells exhibit striking levels of plasticity, as each can regenerate both cell types. Here, we show that thrombin induces a phosphoinositide 3-kinase (PI3K)-Akt pathway-dependent acquisition of DS-like properties by DP cells in vitro, involving increased proliferation rate, acquisition of `myofibroblastic' contractile properties and a decreased capacity to sustain growth and survival of keratinocytes. The thrombin inhibitor protease nexin 1 [PN-1, also known as SERPINE2) regulates all those effects in vitro. Accordingly, the PI3K-Akt pathway is constitutively activated and expression of myofibroblastic marker smooth-muscle actin is enhanced in vivo in hair follicle dermal cells from PN-1–/– mice. Furthermore, physiological PN-1 disappearance and upregulation of the thrombin receptor PAR-1 (also known as F2R) during follicular regression in wild-type mice also correlate with such changes in DP cell characteristics. Our results indicate that control of thrombin signaling interferes with hair follicle dermal cells plasticity to regulate their function.

Key words: PN-1, Thrombin, PI3K pathway, Cell plasticity, Cell differentiation, Hair follicle


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