Apr 22, 2020
Deficiency of CD44 prevents thoracic aortic dissection in a murine model.
Scientific reports
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- Volume
- 10
- Number
- 1
- First page
- 6869
- Last page
- 6869
- Language
- English
- Publishing type
- Research paper (scientific journal)
- DOI
- 10.1038/s41598-020-63824-9
- Publisher
- NATURE PUBLISHING GROUP
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-/-) mice. The incidence of TAD in CD44-/- mice was significantly reduced compared with WT mice (44% and 6%, p < 0.01). Next, to evaluate the initial changes, aortic tissues at 24 hours after BAPN/AngII infusion were examined. Neutrophil accumulation into thoracic aortic adventitia in CD44-/- mice was significantly decreased compared with that in WT mice (5.7 ± 0.3% and 1.6 ± 0.4%, p < 0.01). In addition, BAPN/AngII induced interleukin-6, interleukin-1β, matrix metalloproteinase-2 and matrix metalloproteinase-9 in WT mice, all of which were significantly reduced in CD44-/- mice (all p < 0.01). In vitro transmigration of neutrophils from CD44-/- mice through an endothelial monolayer was significantly decreased by 18% compared with WT mice (p < 0.01). Our findings indicate that CD44 has a critical role in TAD development in association with neutrophil infiltration into adventitia.
- Link information
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- DOI
- https://doi.org/10.1038/s41598-020-63824-9
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/32321956
- PubMed Central
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7176701
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000560329100004&DestApp=WOS_CPL
- Scopus
- https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85083789973&origin=inward Open access
- Scopus Citedby
- https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=85083789973&origin=inward
- ID information
-
- DOI : 10.1038/s41598-020-63824-9
- ISSN : 2045-2322
- eISSN : 2045-2322
- Pubmed ID : 32321956
- Pubmed Central ID : PMC7176701
- SCOPUS ID : 85083789973
- Web of Science ID : WOS:000560329100004