ArticleArteriosclerosis, thrombosis, and vascular biology2010
C-reactive protein-mediated vascular injury requires complement.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 43 citations in OpenAlex.
- Adipsin in the pathogenesis of cardiovascular diseases.Vascular pharmacology · 2024Review
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Recent advances into the role of pattern recognition receptors in transplantation.Cellular immunology · 2020Review
- A Brief Overview of lncRNAs in Endothelial Dysfunction-Associated Diseases: From Discovery to Characterization.Epigenomes · 2019Review
- Perivascular adipose tissue-derived stromal cells contribute to vascular remodeling during aging.Aging cell · 2019Article
- Biomarkers in Cardiorenal Syndromes.BioMed research international · 2018Review
- High Levels of Circulating Endothelial Progenitor Cells Are Associated with Acrotism in Patients with Takayasu Arteritis.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2017Article
- Estrogen and Cardiovascular Disease: Is Timing Everything?The American journal of the medical sciences · 2015Review
- Calreticulin Regulates Neointima Formation and Collagen Deposition following Carotid Artery Ligation.Journal of vascular research · 2015Article
- C-reactive protein induces expression of tissue factor and plasminogen activator inhibitor-1 and promotes fibrin accumulation in vein grafts.Journal of thrombosis and haemostasis : JTH · 2014Article
- Estrogen effects on vascular inflammation are age dependent: role of estrogen receptors.Arteriosclerosis, thrombosis, and vascular biology · 2014Article
- C-reactive protein and hypertension.Journal of human hypertension · 2014Review
- Recognition functions of pentameric C-reactive protein in cardiovascular disease.Mediators of inflammation · 2014Review
- Inhibiting C-reactive protein for the treatment of cardiovascular disease: promising evidence from rodent models.Mediators of inflammation · 2014Article
- The Renin-Angiotensin-aldosterone system in vascular inflammation and remodeling.International journal of inflammation · 2014Review
- Animal models of C-reactive protein.Mediators of inflammation · 2014Review
- Endothelial cell transfusion ameliorates endothelial dysfunction in 5/6 nephrectomized rats.American journal of physiology. Heart and circulatory physiology · 2013Article
- Pentraxins: structure, function, and role in inflammation.ISRN inflammation · 2013Review
- The role of perivascular adipose tissue in vascular smooth muscle cell growth.British journal of pharmacology · 2012Review
- Associations of CFH polymorphisms and CFHR1-CFHR3 deletion with blood pressure and hypertension in Chinese population.PloS one · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWe previously demonstrated that vascular injury-induced neointima formation is exaggerated in human C-reactive protein (CRP) transgenic (CRPtg) compared to nontransgenic (NTG) mice. We now test the hypothesis that complement is required for this effect. METHODS AND
resultsCRPtg and NTG with a normal complement system versus their counterparts lacking expression of complement component 3 (C3) protein (CRPtg/C3(-/-) and NTG/C3(-/-)) underwent carotid artery ligation. Twenty-eight days later, the injured vessels in CRPtg had thicker neointimas and more immunoreactive C3 in the surrounding adventitia compared with NTG. In CRPtg/C3(-/-), there was no increase in neointimal thickness compared with NTG or NTG/C3(-/-). Decreasing human CRP blood levels through administration of a selective antisense oligonucleotide eliminated the depletion of serum C3 associated with vascular injury and reduced immunoreactive C3 in the resultant lesions. In injured vessels, C3 colocalized with F4/80 (macrophage marker), and in vitro, human CRP elicited increased expression of C3 by bone marrow-derived macrophages.
conclusionsHuman CRP exaggeration of neointima formation in injured mouse carotid arteries associates with decreased circulating C3 and increased tissue-localized C3. C3 elimination or pharmacological reduction of human CRP prevents CRP-driven exacerbation of the injury response. In the CRPtg model system, mouse C3 is essential for the effect of human CRP.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.