Epidermal autonomous VEGFA/Flt1/Nrp1 functions mediate psoriasis-like disease.
Animals
Antibodies, Blocking
/ pharmacology
Chromatin Assembly and Disassembly
/ drug effects
Epidermal Cells
/ drug effects
Keratinocytes
/ drug effects
Mice, Knockout
Neuropilin-1
/ metabolism
Phenotype
Proto-Oncogene Proteins c-fos
/ metabolism
Psoriasis
/ genetics
Signal Transduction
/ drug effects
Transcription Factors
/ metabolism
Transcription, Genetic
/ drug effects
Vascular Endothelial Growth Factor A
/ metabolism
Vascular Endothelial Growth Factor Receptor-1
/ metabolism
Journal
Science advances
ISSN: 2375-2548
Titre abrégé: Sci Adv
Pays: United States
ID NLM: 101653440
Informations de publication
Date de publication:
01 2020
01 2020
Historique:
received:
05
04
2019
accepted:
11
11
2019
entrez:
15
1
2020
pubmed:
15
1
2020
medline:
18
9
2020
Statut:
epublish
Résumé
Psoriasis is a common chronic skin disorder characterized by keratinocyte hyperproliferation with altered differentiation accompanied by inflammation and increased angiogenesis. It remains unclear whether the first events that initiate psoriasis development occur in keratinocytes or inflammatory cells. Here, using different psoriasis mouse models, we showed that conditional deletion of
Identifiants
pubmed: 31934626
doi: 10.1126/sciadv.aax5849
pii: aax5849
pmc: PMC6949033
doi:
Substances chimiques
Antibodies, Blocking
0
JunB protein, mouse
0
Proto-Oncogene Proteins c-fos
0
Transcription Factors
0
Vascular Endothelial Growth Factor A
0
fos-related antigen 1
0
Neuropilin-1
144713-63-3
Flt1 protein, mouse
EC 2.7.10.1
Vascular Endothelial Growth Factor Receptor-1
EC 2.7.10.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
eaax5849Informations de copyright
Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).
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