Apelin/APJ signaling suppresses the pressure ulcer formation in cutaneous ischemia-reperfusion injury mouse model.
Animals
Apelin
/ genetics
Apelin Receptors
/ genetics
Apoptosis
/ genetics
Cytokines
/ genetics
Disease Models, Animal
Fluorescent Antibody Technique
Gene Expression
Mice
Oxidative Stress
Reactive Oxygen Species
/ metabolism
Reperfusion Injury
/ etiology
Signal Transduction
Skin
/ blood supply
Ulcer
/ etiology
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
28 Jan 2020
28 Jan 2020
Historique:
received:
15
08
2019
accepted:
15
01
2020
entrez:
30
1
2020
pubmed:
30
1
2020
medline:
11
6
2020
Statut:
epublish
Résumé
Several studies have demonstrated potential roles for apelin/APJ signaling in the regulation of oxidative stress associated with ischemia-reperfusion (I/R) injury in several organs. Objective was to assess the role of apelin/APJ signaling in the development of pressure ulcers (PUs) formation after cutaneous I/R injury in mice. We identified that cutaneous I/R injury increased the expression of apelin in the skin at I/R site. Administration of apelin significantly inhibited the formation of PUs. The reductions of blood vessels, hypoxic area and apoptosis in I/R site were inhibited by apelin injection. Oxidative stress signals in OKD48 mice and the expressions of oxidative stress related genes in the skin were suppressed by apelin injection. H
Identifiants
pubmed: 31992828
doi: 10.1038/s41598-020-58452-2
pii: 10.1038/s41598-020-58452-2
pmc: PMC6987197
doi:
Substances chimiques
Apelin
0
Apelin Receptors
0
Apln protein, mouse
0
Aplnr protein, mouse
0
Cytokines
0
Reactive Oxygen Species
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1349Références
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