ArticleBMC musculoskeletal disorders2001
MCMV induces neointima in IFN-gammaR-/- mice: intimal cell apoptosis and persistent proliferation of myofibroblasts.
Article in BMC musculoskeletal disorders, 2001. 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.
- Similarities between COVID-19 and systemic sclerosis early vasculopathy: A "viral" challenge for future research in scleroderma.Autoimmunity reviews · 2021Review
- Article
- Identification and Validation of Key Genes Associated With Systemic Sclerosis-Related Pulmonary Hypertension.Frontiers in genetics · 2020Article
- Infections as a cause of autoimmune rheumatic diseases.Auto- immunity highlights · 2016Review
- Localized cutaneous sclerodermoid changes secondary to human cytomegalovirus infection: An uncommon presentation in an immunocompetent host.JAAD case reports · 2016Article
- Fresh Insights into Disease Etiology and the Role of Microbial Pathogens.Current rheumatology reports · 2016Review
- Human cytomegalovirus and autoimmune disease.BioMed research international · 2014Review
- Updates on morphea: role of vascular injury and advances in treatment.Autoimmune diseases · 2013Review
- CD13/aminopeptidase N and murine cytomegalovirus infection.Virology · 2005Article
- Animal models for scleroderma: an update.Current rheumatology reports · 2002Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCMV infections have been linked to vasculopathies like atherosclerosis and Scleroderma. CMV infects vascular endothelium with intermittent shedding of the virus and the development of latency.
methodsWe adopted a model of arteritis, developed by Presti et al. (1998), triggered by murine cytomegalovirus (MCMV) infection. Our studies focused on neointima formation. Groups of mice include: 1) immunocompetent 129S, 2) immunocompetent 129S receiving whole body irradiation and MCMV, 3) IFN-gammaR-/- receiving MCMV, and 4) IFN-gammaR-/- receiving MCMV and whole body irradiation.
resultsMice were inoculated with MCMV (5 x 10(4) or 1 x 10(5) PFU's) by i.p. injection; hearts and abdominal aortas were collected and histopathology evaluated. Infected immunocompetent animals exhibited widespread perivascular inflammation, which subsided by 8 weeks. Intimal pathology was not observed in any control group. Immunocompetent animals receiving MCMV and irradiation developed mild to moderate intimal lesions associated with medial and adventitial inflammation. IFN-gammaR-/- mice infected for 4 months and receiving whole body irradiation 2 months after infection developed pathology characterized by extensive adventitial and medial infiltrate and significant neointima, suggesting that infection and immunosuppression were co-requisites of neointima formation. Immunohistochemical analysis revealed myofibroblasts as a major component of neointima. The disease is characterized by up-regulation of growth factors (TGF-beta1, PDGF-A and B). Apoptosis was detected in the intimal layer of affected aortas. Active proliferation of myofibroblasts and infiltrating cells was also detected.
conclusionThese results indicate that CMV infections may lead to intimal injury that results in the formation of neointima characteristic of autoimmune vasculopathies.
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Registered trials
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