The role of LEKTI in fate determination of keratinocyte stem cells

Details

Serval ID
serval:BIB_726E87D30DFD
Type
Inproceedings: an article in a conference proceedings.
Publication sub-type
Abstract (Abstract): shot summary in a article that contain essentials elements presented during a scientific conference, lecture or from a poster.
Collection
Publications
Institution
Title
The role of LEKTI in fate determination of keratinocyte stem cells
Title of the conference
16th International Conference on the International Society of Differentiation
Author(s)
Amici A.W., Volorio C., Rochat A., Hovnanian A., Barrando Y.
Address
Nara, Japan, November 15-18, 2010
ISBN
0301-4681
Publication state
Published
Issued date
2010
Peer-reviewed
Oui
Volume
80
Series
Differentiation
Pages
S45-S46
Language
english
Notes
Publication type : Meeting Abstract
Abstract
SPINK5 (serine protease inhibitor Kazal-type 5) encodes the putative proteinase inhibitor LEKTI (lympho-epithelial Kazal-type related inhibitor). In skin, LEKTI expression is restricted to the stratum granulosum of the epidermis and the inner root sheath of hair follicles. Mutations that create premature termination codons in SPINK5 have been reported as the cause of Netherton syndrome (NS), a human autosomal recessive disorder characterized by congenital ichthyosis with defective cornification, a specific hair shaft defect known as trichorrexis invaginata or 'bamboo hair', and severe atopic manifestations, including atopic dermatitis and hayfever. Althought recombinant human LEKTI inhibits a battery of serine proteases including plasmin, trypsin, subtilisin A, cathepsin G, and elastase, the precise role of LEKTI in the physiopathology of NS remains unclear. Spink5−/− mice display a NS-like phenotype. Surprisingly, a psoriasis-like hyperplasia, basement membrane breakdown followed by evagination of spindle-shaped epidermal cells into the dermal compartment, and the presence of numerous sweat gland-like structures were also observed when the skin of Spink5−/− newborn mice, which die at birth, was transplanted onto the back of nude mice. Collectively, these observations suggest that LEKTI may play a role on cell proliferation and stem cell fate. Our current work aims at elucidating the mechanisms by which LEKTI impact these biological processes. Using keratinocyte stem cells obtained from NS patients, we have identified LEKTI as a regulator node in several signaling pathways involved in stem cell behavior.
Keywords
,
Web of science
Create date
20/01/2011 12:43
Last modification date
20/08/2019 15:30
Usage data