ArticleThe Journal of clinical investigation1998
Reduced transplant arteriosclerosis in plasminogen-deficient mice.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 91 citations in OpenAlex.
- Plasminogen as a ribonucleoprotein: regulatory small RNA cargo modulates fibrinolysis and inflammation.Blood · 2025Article
- A Serine Protease Inhibitor, Camostat Mesilate, Suppresses Urinary Plasmin Activity and Alleviates Hypertension and Podocyte Injury in Dahl Salt-Sensitive Rats.International journal of molecular sciences · 2023Article
- Difference in Biomarkers Between COVID-19 Patients and Other Pulmonary Infection Patients.Infection and drug resistance · 2020Article
- Plasmin-mediated fibrinolysis enables macrophage migration in a murine model of inflammation.Blood · 2019Article
- Lp(a)/apo(a) modulate MMP-9 activation and neutrophil cytokines in vivo in inflammation to regulate leukocyte recruitment.The American journal of pathology · 2014Article
- Plasmin promotes foam cell formation by increasing macrophage catabolism of aggregated low-density lipoprotein.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- Plasminogen controls inflammation and pathogenesis of influenza virus infections via fibrinolysis.PLoS pathogens · 2013Article
- Article
- L-type calcium channel blockers exert an antiinflammatory effect by suppressing expression of plasminogen receptors on macrophages.Circulation research · 2009Article
- Plasminogen mediates the atherogenic effects of macrophage-expressed urokinase and accelerates atherosclerosis in apoE-knockout mice.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Inflammatory macrophage migration requires MMP-9 activation by plasminogen in mice.The Journal of clinical investigation · 2008Article
- Article
- Alterations in the fibrinolytic cascade post-transplant: evidence of a bimodal expression pattern.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2007Article
- Article
- Mouse models of arteriosclerosis: from arterial injuries to vascular grafts.The American journal of pathology · 2004Review
- Deficiency of cathepsin S reduces atherosclerosis in LDL receptor-deficient mice.The Journal of clinical investigation · 2003Article
- Remodeling of the vessel wall after copper-induced injury is highly attenuated in mice with a total deficiency of plasminogen activator inhibitor-1.The American journal of pathology · 2001Article
- The role of proteinases in angiogenesis, heart development, restenosis, atherosclerosis, myocardial ischemia, and stroke: insights from genetic studies.Current atherosclerosis reports · 2000Review
- Suppressed smooth muscle proliferation and inflammatory cell invasion after arterial injury in elafin-overexpressing mice.The Journal of clinical investigation · 2000Article
- Proteinases in cardiovascular aneurysms and rupture: targets for therapy?The Journal of clinical investigation · 2000Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Recent gene targeting studies indicate that the plasminogen system is implicated in cell migration and matrix degradation during arterial neointima formation and atherosclerotic aneurysm formation. This study examined whether plasmin proteolysis is involved in accelerated posttransplant arteriosclerosis (graft arterial disease). Donor carotid arteries from wild-type B10.A2R mice were transplanted into either plasminogen wild-type (Plg+/+) or homozygous plasminogen-deficient (Plg-/-) recipient mice with a genetic background of 75% C57BL/6 and 25% 129. Within 15 d after allograft transplantation, leukocytes and macrophages infiltrated the graft intima in Plg+/+ and Plg-/- recipient mice to a similar extent. In Plg+/+ recipients, the elastic laminae in the transplant media exhibited breaks through which macrophages infiltrated before smooth muscle cell proliferation, whereas in Plg-/- recipients, macrophages failed to infiltrate the transplant media which remained structurally more intact. After 45 d of transplantation, a multilayered smooth muscle cell-rich transplant neointima developed in Plg+/+ hosts, in contrast to Plg-/- recipients, in which the transplants contained a smaller intima, predominantly consisting of leukocytes, macrophages, and thrombus. Media necrosis, fragmentation of the elastic laminae, and adventitial remodeling were more pronounced in Plg+/+ than in Plg-/- recipient mice. Expression of the plasminogen activators (PA), urokinase-type PA (u-PA) and tissue-type PA (t-PA), and expression of the matrix metalloproteinases (MMPs), MMP-3, MMP-9, MMP-12, and MMP-13, were significantly increased within 15 d of transplantation when cells actively migrate. These data indicate that plasmin proteolysis plays a major role in allograft arteriosclerosis by mediating elastin degradation, macrophage infiltration, media remodeling, medial smooth muscle cell migration, and formation of a neointima.
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