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

Details

Serval ID
serval:BIB_96701495A5BB
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Control of thrombin signaling through PI3K is a mechanism underlying plasticity between hair follicle dermal sheath and papilla cells.
Journal
Journal of Cell Science
Author(s)
Feutz A.C., Barrandon Y., Monard D.
ISSN
0021-9533
Publication state
Published
Issued date
2008
Peer-reviewed
Oui
Volume
121
Number
Pt 9
Pages
1435-1443
Language
english
Abstract
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.
Keywords
1-Phosphatidylinositol 3-Kinase, Amyloid beta-Protein Precursor, Animals, Cell Proliferation, Cells, Cultured, Dermis, Enzyme Activation, Fibroblasts, Hair Follicle, Mice, Phenotype, Protein Transport, Proto-Oncogene Proteins c-akt, Receptors, Cell Surface, Signal Transduction, Thrombin
Pubmed
Web of science
Open Access
Yes
Create date
25/02/2009 9:46
Last modification date
20/08/2019 14:58
Usage data