ArticlePloS one2013
Knockout of CD8 delays reendothelialization and accelerates neointima formation in injured arteries of mouse via TNF-α inhibiting the endothelial cells migration.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Novel Paracrine Functions of Smooth Muscle Cells in Supporting Endothelial Regeneration Following Arterial Injury.Circulation research · 2019Article
- Involvement of CD8+ T cell subsets in early response to vascular injury in patients with peripheral artery disease in vivo.Clinical immunology (Orlando, Fla.) · 2018Article
- Identification of type IV collagen exposure as a molecular imaging target for early detection of thoracic aortic dissection.Theranostics · 2018Article
- Accelerated atherogenesis in completely ligated common carotid artery of apolipoprotein E-deficient mice.Oncotarget · 2017Article
- Article
- CD40 in coronary artery disease: a matter of macrophages?Basic research in cardiology · 2016Review
- PTP1B inhibitor promotes endothelial cell motility by activating the DOCK180/Rac1 pathway.Scientific reports · 2016Article
- In Vivo siRNA Delivery Using JC Virus-like Particles Decreases the Expression of RANKL in Rats.Molecular therapy. Nucleic acids · 2016Article
- Curcumin accelerates reendothelialization and ameliorates intimal hyperplasia in balloon-injured rat carotid artery via the upregulation of endothelial cell autophagy.International journal of molecular medicine · 2015Article
- Article
- Hydroxysafflor yellow A inhibits lipopolysaccharide-induced proliferation and migration of vascular smooth muscle cells via Toll-like receptor-4 pathway.International journal of clinical and experimental medicine · 2015Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveDelayed or impaired reendothelialization is a major cause of stent thrombosis in the interventional treatment of coronary heart disease. T cells are involved in neointima formation of injured arteries. However, the regulated mechanism of reendothelialization and the role of CD8 T cell in reendothelialization are unclear. METHODS AND
resultsImmunofluorescence staining showed that CD8 positive cells were increased in wire injured femoral artery of mice. On day 21 after injury, elastin staining showed that knockout of CD8 (CD8(-/-)) significantly increased intimal thickness and a ratio of intima to media by 1.8 folds and 1.9 folds respectively in injured arteries. Evans blue staining showed that knockout of CD8 delayed the reendothelialization area on day 7 after injury (18.8±0.5% versus 42.1±5.6%, p<0.05). In vitro, a migration assay revealed that CD8(-/-) T cells co-cultured with WT macrophages significantly inhibited the migration of the endothelial cells (ECs); compared to CD4(+) T cells, and CD8(+) T cells could promote the ECs migration. Furthermore, real-time PCR analysis showed that knockout of CD8 increased the level of tumor necrosis factor α (TNF-α) in injured arteries and cytometric bead cytokine array showed that TNF-α was elevated in cultured CD8(-/-) T cells. Finally, a wound-healing assay showed that recombinant TNF-α significantly inhibited the migration of ECs.
conclusionOur study suggested that CD8(+) T cells could promote the reendothelialization and inhibit the neointima formation after the artery wire injury, and this effect is at least partly dependent on decreasing TNF-α production promoting ECs migration.
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