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@ARTICLE{Pichery:124272,
author = {M. Pichery and A. Huchenq and R. Sandhoff$^*$ and M.
Severino-Freire and S. Zaafouri and L. Opálka and T. Levade
and V. Soldan and J. Bertrand-Michel and E. Lhuillier and G.
Serre and A. Maruani and J. Mazereeuw-Hautier and N. Jonca},
title = {{PNPLA}1 defects in patients with autosomal recessive
congenital ichthyosis and {KO} mice sustain {PNPLA}1
irreplaceable function in epidermal omega-{O}-acylceramide
synthesis and skin permeability barrier.},
journal = {Human molecular genetics},
volume = {26},
number = {10},
issn = {1460-2083},
address = {Oxford},
publisher = {Oxford Univ. Press},
reportid = {DKFZ-2017-01168},
pages = {1787 - 1800},
year = {2017},
abstract = {Autosomal recessive congenital ichthyosis (ARCI) is a
heterogeneous group of monogenic genodermatoses that
encompasses non-syndromic disorders of keratinization. The
pathophysiology of ARCI has been linked to a disturbance in
epidermal lipid metabolism that impaired the stratum corneum
function, leading to permeability barrier defects.
Functional characterization of some genes involved in ARCI
contributed to the identification of molecular actors
involved in epidermal lipid synthesis, transport or
processing. Recently, PNPLA1 has been identified as a gene
causing ARCI. While other members of PNPLA family are key
elements in lipid metabolism, the function of PNPLA1
remained unclear. We identified 5 novel PNPLA1 mutations in
ARCI patients, mainly localized in the putative active
enzymatic domain of PNPLA1. To investigate Pnpla1 biological
role, we analysed Pnpla1-deficient mice. KO mice died soon
after birth from severe epidermal permeability defects.
Pnpla1-deficient skin presented an important impairment in
the composition and organization of the epidermal lipids.
Quantification of epidermal ceramide species highlighted a
blockade in the production of ω-O-acylceramides with a
concomitant accumulation of their precursors in the KO. The
virtually loss of ω-O-acylceramides in the stratum corneum
was linked to a defective lipid coverage of the resistant
pericellular shell encapsulating corneocytes, the so-called
cornified envelope, and most probably disorganized the
extracellular lipid matrix. Finally, these defects in
ω-O-acylceramides synthesis and cornified envelope
formation were also evidenced in the stratum corneum from
PNPLA1-mutated patients. Overall, our data support that
PNPLA1/Pnpla1 is a key player in the formation of
ω-O-acylceramide, a crucial process for the epidermal
permeability barrier function.},
cin = {G131},
ddc = {570},
cid = {I:(DE-He78)G131-20160331},
pnm = {317 - Translational cancer research (POF3-317)},
pid = {G:(DE-HGF)POF3-317},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:28369476},
doi = {10.1093/hmg/ddx079},
url = {https://inrepo02.dkfz.de/record/124272},
}