ArticlePloS one2013
The Nogo-B-PirB axis controls macrophage-mediated vascular remodeling.
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 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
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- PD-L1 (Programmed Death Ligand 1) Regulates T-Cell Differentiation to Control Adaptive Venous Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Inhibition of T-Cells by Cyclosporine A Reduces Macrophage Accumulation to Regulate Venous Adaptive Remodeling and Increase Arteriovenous Fistula Maturation.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Macrophage Paired Immunoglobulin-Like Receptor B Deficiency Promotes Peripheral Atherosclerosis in Apolipoprotein E-Deficient Mice.Frontiers in cell and developmental biology · 2021Article
- Impact of RTN4 gene polymorphism and its plasma level on susceptibility to nasopharyngeal carcinoma: A case-control study.Medicine · 2019Article
- Inhibition of the Akt1-mTORC1 Axis Alters Venous Remodeling to Improve Arteriovenous Fistula Patency.Scientific reports · 2019Article
- Mineralocorticoid receptor: A hidden culprit for hemodialysis vascular access dysfunction.EBioMedicine · 2019Review
- Nogo-B promotes tumor angiogenesis and provides a potential therapeutic target in hepatocellular carcinoma.Molecular oncology · 2018Article
- CD44 Promotes Inflammation and Extracellular Matrix Production During Arteriovenous Fistula Maturation.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Pretreatment of pericardial patches with antibiotics does not alter patch healing in vivo.Journal of vascular surgery · 2016Article
- Yiqihuoxuejiedu Formula Restrains Vascular Remodeling by Reducing the Inflammation Reaction and Cx43 Expression in the Adventitia after Balloon Injury.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Adjusting the compass: new insights into the role of angiogenesis in Alzheimer's disease.Alzheimer's research & therapy · 2013Review
- Autologous tissue patches acquire vascular identity depending on the environment.Vascular investigation and therapyArticle
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
objectiveNogo-B mediates vascular protection and facilitates monocyte- and macrophage-dependent vascular remodeling. PirB is an alternate receptor for Nogo-B, but a role for the Nogo-PirB axis within the vascular system has not been previously reported. We examined whether Nogo-B or PirB play a role in regulating macrophage-mediated vascular remodeling and hypothesized that endothelial Nogo-B regulates vein graft macrophage infiltration via its alternate receptor PirB.
methodsVein grafts were performed using Nogo and PirB wild type and knockout mice. Human vein grafts were similarly analyzed. The hindlimb ischemia model was performed in PirB wild type and knockout mice. Accompanying in vitro work included isolation of macrophages from PirB wild type and knockout mice.
resultsIncreased Nogo-B and PirB mRNA transcripts and protein expression were observed within mouse and human vein grafts. Both Nogo knockout and PirB knockout vein grafts showed increased wall thickness and increased numbers of F4/80-positive macrophages. Macrophages derived from PirB knockout mice had increased adhesion to fibronectin, increased EC-specific binding, and increased numbers of mRNA transcripts of M2 markers as well as MMP3 and MMP9. PirB knockout vein grafts had increased active MMP9 compared to wild type vein grafts. PirB knockout mice had increased recovery from hindlimb ischemia and increased macrophage infiltration compared to wild type mice.
conclusionsVein graft adaptation shows increased expression of both Nogo-B and PirB. Loss of PirB, or its endothelial ligand Nogo-B, results in increased inflammatory cell infiltration and vein graft wall thickening. These findings suggest that PirB regulates macrophage activity in vein grafts and that Nogo-B in the vein graft limits macrophage infiltration and vein graft thickening. PirB may play a more general role in regulating macrophage responses to vascular injury. Macrophage inhibition via Nogo-PirB interactions may be an important mechanism regulating vein graft adaptation to the arterial circulation.
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