ArticleExperimental animals2019
Involvement of B cells in the pathophysiology of β-aminopropionitrile-induced thoracic aortic dissection in mice.
Article in Experimental animals, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Mouse models of aortic dissection induced by β-aminopropionitrile combined with angiotensin II and the changes in their gut microbiota.BMC microbiology · 2025Article
- Transcriptome-Based Identification of Biomarkers Associated With Sphingosine-1-Phosphate Signaling Pathway in Aortic Dissection.International journal of hypertension · 2025Article
- β-Aminopropionitrile Induces Distinct Pathologies in the Ascending and Descending Thoracic Aortic Regions of Mice.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- β-aminopropionitrile Induces Distinct Pathologies in the Ascending and Descending Thoracic Aortic Regions of Mice.bioRxiv : the preprint server for biology · 2024Article
- Independent and Interactive Roles of Immunity and Metabolism in Aortic Dissection.International journal of molecular sciences · 2023Review
- Mechanistic insight into lysyl oxidase in vascular remodeling and angiogenesis.Genes & diseases · 2023Review
- Identification of FERMT1 and SGCD as key marker in acute aortic dissection from the perspective of predictive, preventive, and personalized medicine.The EPMA journal · 2022Article
- β-Aminopropionitrile-induced aortic aneurysm and dissection in mice.JVS-vascular science · 2022Review
- Patterns of Immune Infiltration and the Key Immune-Related Genes in Acute Type A Aortic Dissection in Bioinformatics Analyses.International journal of general medicine · 2021Article
- Induction of thoracic aortic dissection: a mini-review of β-aminopropionitrile-related mouse models.Journal of Zhejiang University. Science. BReview
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10 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Thoracic aortic dissection (TAD) is a life-threatening disease that is characterized by an inflammatory response. Innate and cellular immunity has long been known to be involved in TAD, but the role of humoral immunity in the pathophysiology of TAD remains unknown. We administered the lysyl oxidase inhibitor β-aminopropionitrile (BAPN; 1 g/kg/day) in 3-week-old male C57BL/6J mice for 4 weeks to establish an animal model of TAD. Animals that died were immediately dissected. Animals that survived were sacrificed on days 7, 14, and 28 after BAPN challenge. The incidence and rupture rates of BAPN-induced TAD were 90% (9/10) and 70% (7/10), respectively, at 28 days. Victoria blue-nuclear fast red staining of aortic tissue revealed elastic lamellae destruction and the formation of a false lumen in the BAPN group. Hematoxylin-eosin staining revealed the infiltration of both plasmacytoid mononuclear cells and polymorphonuclear inflammatory cells in TAD tissues. Enzyme-linked immunosorbent assay and immunohistochemistry indicated that plasma immunoglobin M (IgM) and IgG were elevated at 7, 14, and 28 days, and CD19-positive B cells infiltrated into the adventitia of aortic tissue in BAPN-treated mice. The transcriptional analysis showed an increase in the expression of B cell receptor signaling-associated genes. These results indicate that B cells and immunoglobulins might participate in the pathogenesis of TAD, suggesting that humoral immunity may be a possible therapeutic target for TAD.
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