Activation of the C3a anaphylatoxin receptor inhibits keratinocyte proliferation by regulating keratin 6, keratin 16, and keratin 17 in psoriasis.
C3a anaphylatoxin receptor
complement
downregulation
keratin
proliferation
psoriasis
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
05 2022
05 2022
Historique:
revised:
29
03
2022
received:
17
09
2021
accepted:
07
04
2022
entrez:
16
4
2022
pubmed:
17
4
2022
medline:
20
4
2022
Statut:
ppublish
Résumé
Emerging evidence suggests that signaling through the C3a anaphylatoxin receptor (C3aR) protects against various inflammation-related diseases. However, the role of C3aR in psoriasis remains unknown. The purpose of this study was to investigate the possible protective role of C3aR in psoriasis and to explore the underlying molecular mechanisms. We initially found that the psoriatic epidermis exhibited significantly decreased C3aR expression. C3aR showed protective roles in mouse models of imiquimod (IMQ)- and interleukin-23-induced psoriasis. Furthermore, increased epidermal thickness and keratin 6 (K6), K16, and K17 expression occurred in the ears and backs of C3aR
Identifiants
pubmed: 35429062
doi: 10.1096/fj.202101458R
doi:
Substances chimiques
Anaphylatoxins
0
C3a-derived anaphylatoxin receptor, mouse
0
Keratin-16
0
Keratin-17
0
Keratin-6
0
Receptors, G-Protein-Coupled
0
Keratins
68238-35-7
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e22322Informations de copyright
© 2022 The Authors. The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.
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