Deficiency of CD44 prevents thoracic aortic dissection in a murine model.
Aminopropionitrile
/ adverse effects
Aortic Dissection
/ chemically induced
Angiotensin II
/ adverse effects
Animals
Aortic Aneurysm, Thoracic
/ chemically induced
Disease Models, Animal
Endothelium, Vascular
/ metabolism
Gene Expression Regulation
Humans
Hyaluronan Receptors
/ deficiency
Mice
Mice, Knockout
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
22 04 2020
22 04 2020
Historique:
received:
29
11
2019
accepted:
07
04
2020
entrez:
24
4
2020
pubmed:
24
4
2020
medline:
25
11
2020
Statut:
epublish
Résumé
Thoracic aortic dissection (TAD) is a life-threatening vascular disease. We showed that CD44, a widely distributed cell surface adhesion molecule, has an important role in inflammation. In this study, we examined the role of CD44 in the development of TAD. TAD was induced by the continuous infusion of β-aminopropionitrile (BAPN), a lysyl oxidase inhibitor, and angiotensin II (AngII) for 7 days in wild type (WT) mice and CD44 deficient (CD44
Identifiants
pubmed: 32321956
doi: 10.1038/s41598-020-63824-9
pii: 10.1038/s41598-020-63824-9
pmc: PMC7176701
doi:
Substances chimiques
Cd44 protein, mouse
0
Hyaluronan Receptors
0
Angiotensin II
11128-99-7
Aminopropionitrile
151-18-8
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
6869Références
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