Autocrine regulation of wound healing by ATP release and P2Y


Journal

Life sciences
ISSN: 1879-0631
Titre abrégé: Life Sci
Pays: Netherlands
ID NLM: 0375521

Informations de publication

Date de publication:
15 Oct 2021
Historique:
received: 22 02 2021
revised: 05 07 2021
accepted: 17 07 2021
pubmed: 28 7 2021
medline: 14 9 2021
entrez: 27 7 2021
Statut: ppublish

Résumé

Application of exogenous nucleotides can modulate wound healing via the activation of purinergic receptors. However, evidence for the release of endogenous nucleotides and the subsequent activation of purinergic receptors in this process has not been well defined. Therefore, the current study aimed to investigate wound-mediated nucleotide release and autocrine purinergic signalling during HaCaT keratinocyte wound closure following scratch injury. An in vitro scratch wound apparatus was employed to study wound healing over 24-h in the presence of modulators of ATP release, P2 receptors and pathways downstream of P2 receptor activation. Adenosine 5'-triphosphate (ATP) was released from scratched cells. The ectonucleotidase apyrase and pharmacological inhibition of the nucleotide release hemichannel, pannexin-1, decreased wound closure over time. The non-selective P2Y receptor antagonist suramin and the selective P2Y These data describe a novel autocrine signalling mechanism in which wound-mediated release of endogenous ATP in response to mechanical scratching of HaCaT cells activates P2Y

Identifiants

pubmed: 34314735
pii: S0024-3205(21)00837-7
doi: 10.1016/j.lfs.2021.119850
pii:
doi:

Substances chimiques

P2RY2 protein, human 0
Purinergic P2Y Receptor Antagonists 0
Receptors, Purinergic P2Y2 0
Suramin 6032D45BEM
Adenosine Triphosphate 8L70Q75FXE

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

119850

Informations de copyright

Copyright © 2021 Elsevier Inc. All rights reserved.

Auteurs

T B-D McEwan (TB)

Illawarra Health and Medical Research Institute, Wollongong, NSW 2522, Australia; Molecular Horizons and School of Chemistry and Molecular Bioscience, University of Wollongong, Wollongong, NSW 2522, Australia.

R A Sophocleous (RA)

Illawarra Health and Medical Research Institute, Wollongong, NSW 2522, Australia; Molecular Horizons and School of Chemistry and Molecular Bioscience, University of Wollongong, Wollongong, NSW 2522, Australia.

P Cuthbertson (P)

Illawarra Health and Medical Research Institute, Wollongong, NSW 2522, Australia; Molecular Horizons and School of Chemistry and Molecular Bioscience, University of Wollongong, Wollongong, NSW 2522, Australia.

K J Mansfield (KJ)

Illawarra Health and Medical Research Institute, Wollongong, NSW 2522, Australia; School of Medicine, University of Wollongong, Wollongong, NSW 2522, Australia.

M L Sanderson-Smith (ML)

Illawarra Health and Medical Research Institute, Wollongong, NSW 2522, Australia; Molecular Horizons and School of Chemistry and Molecular Bioscience, University of Wollongong, Wollongong, NSW 2522, Australia.

R Sluyter (R)

Illawarra Health and Medical Research Institute, Wollongong, NSW 2522, Australia; Molecular Horizons and School of Chemistry and Molecular Bioscience, University of Wollongong, Wollongong, NSW 2522, Australia. Electronic address: rsluyter@uow.edu.au.

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Classifications MeSH