C-reactive protein: The pawn has been promoted to queen

Yeh, Edward T.H.; Palusiński, Robert

doi:10.1007/s11883-003-0080-4

Cited by 30 publications

(20 citation statements)

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“…3,4 This could be in part the result of some of the biological properties of CRP such as its stability, lack of diurnal variation, and lack of influence of gender and age. 10 However, accumulating evidence also points to the possibility that CRP is a direct participant in vascular inflammation. 16 One of the outstanding unresolved issues in this field is the source of CRP production in humans.…”

Section: Discussionmentioning

confidence: 99%

“…[5][6][7][8][9] CRP, named for its capacity to bind to the C-polysaccharide of Streptococcus pneumoniae, was the first acute-phase protein to be described. 10 CRP, like other acute-phase proteins, is synthesized by the liver in response to microbial infection, tissue injury, and autoimmune disorders. It had been shown that interleukin-1␤ (IL-1␤) and IL-6 strongly induced the expression of CRP in human hepatocytes 11 and hepatoma cells.…”

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confidence: 99%

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Inflammatory Cytokines Stimulated C-Reactive Protein Production by Human Coronary Artery Smooth Muscle Cells

2003

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Background-Serum C-reactive protein (CRP) levels are good predictors of the development of cardiovascular events in apparently healthy men and women. CRP has been believed to be produced exclusively by hepatocytes during the acute-phase response. Several lines of evidence have suggested that atherosclerotic arteries can also produce CRP. However, the cell types that produce CRP locally in the atherosclerotic arterial wall have not been clearly identified. Methods and Results-Human coronary artery smooth muscle cells (HCASMCs) and human umbilical vein endothelial cells (HUVECs) were incubated with interleukin-1␤ (IL-1␤), IL-6, their combination, tumor necrosis factor-␣ (TNF-␣), or lipopolysaccharide (LPS) at different concentrations. The supernatants were concentrated and analyzed by a high-sensitivity enzyme-linked immunosorbent assay specific for human CRP. RNA was extracted from the HCASMCs for reverse transcriptase-polymerase chain reaction (RT-PCR) using specific primers for the CRP. Maximal CRP production was observed in HCASMCs after 48 hours of incubation with the combination of 25 ng/mL of IL-1␤ and 10 ng/mL of IL-6, whereas incubation with IL-1␤ or IL-6 alone only modestly induced CRP. Incubation with TNF-␣ (50 ng/mL) or LPS (1000 EU/mL) resulted in an increase in CRP production comparable to the IL-1␤ and IL-6 combination. [1][2][3][4] and could directly participate in the pathogenesis of atherosclerosis through activation of endothelial cells. 5-9 CRP, named for its capacity to bind to the C-polysaccharide of Streptococcus pneumoniae, was the first acute-phase protein to be described. 10 CRP, like other acute-phase proteins, is synthesized by the liver in response to microbial infection, tissue injury, and autoimmune disorders. It had been shown that interleukin-1␤ (IL-1␤) and IL-6 strongly induced the expression of CRP in human hepatocytes 11 and hepatoma cells. 12 Recently, human neuronal cells were found to produce CRP in Alzheimer's disease. 13 In addition, renal cortical tubular epithelial cells were shown to produce CRP after inflammatory stimuli. 14 Interestingly, CRP has also been found in human atherosclerotic plaques, 15 which could be the result of indirect deposit from circulating cells or direct production by cells in the arterial wall. We show that human coronary artery smooth muscle cells (HCASMCs), but not human umbilical vein endothelial cells (HUVECs), can synthesize CRP after stimulation by inflammatory cytokines. Methods Cell CultureHCASMCs, HUVECs, and endothelial cell supplements were purchased from Cascade Biologics; penicillin, streptomycin, medium 231, medium 199, and smooth muscle cell growth supplement were from Gibco BRL; and fetal bovine serum, human serum, heparin, and gelatin were obtained from Sigma. HCASMCs were plated onto 0.1% gelatin-coated culture dishes from Corning, Inc, and grown in 231 medium with growth supplement and 1% penicillin/streptomycin; HUVECs were plated onto 0.1% gelatin-coated culture dishes and grown in 199 medium with endothelial growth suppleme...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Inflammatory Cytokines Stimulated C-Reactive Protein Production by Human Coronary Artery Smooth Muscle Cells

2003

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“…C-reactive protein is present in trace levels in healthy individuals and at extremely high levels in the presence of infections, autoimmune diseases, and cancer. 12,13 Levels of CRP that may be predictive of cardiovascular risk can be as low as 1 mg/l and are measured by widely available high-sensitivity assays. 12,14 High-sensitivity CRP (hs-CRP) has shown strong predictive ability in patients with known CVD.…”

Section: C-reactive Protein and Cardiovascular Risk Predictionmentioning

confidence: 99%

“…12,13 Levels of CRP that may be predictive of cardiovascular risk can be as low as 1 mg/l and are measured by widely available high-sensitivity assays. 12,14 High-sensitivity CRP (hs-CRP) has shown strong predictive ability in patients with known CVD. In one of the earliest studies, patients with unstable angina and levels of CRP and serum amyloid A ≥ 3 mg/l averaged 4.8 ischemic episodes during hospitalization, significantly more than those with acute-phase reactants < 3 mg/l, who averaged only 1.8 episodes (p = 0.004).…”

Section: C-reactive Protein and Cardiovascular Risk Predictionmentioning

confidence: 99%

“…1,6,7 C-reactive protein has predicted new and recurrent events in patients with established atherosclerosis and is linked increasingly to the metabolic syndrome and diabetes mellitus. [8][9][10] It now appears that CRP plays a direct role in atherogenesis, 11,12 and approaches to the medical management of CRP are being studied, even as its optimal role in risk assessment is taking shape.…”

Section: Introductionmentioning

confidence: 99%

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High-sensitivity C-reactive protein as a risk assessment tool for cardiovascular disease

Yeh

2005

Clin Cardiol

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Summary: Almost half of first cardiovascular events occur in individuals with no known risk factors. Attempts in the last decade to predict cardiovascular risk more accurately have led to the emergence of a novel risk factor, C-reactive protein (CRP), which has proved to be as good a risk predictor as lowdensity lipoprotein cholesterol. C-reactive protein is an index of inflammation that is now believed to promote directly all stages of atherosclerosis, including plaque rupture. As measured by high-sensitivity assays, high-sensitivity CRP (hs-CRP) also independently predicts recurrent events in patients with known coronary artery diseases. Recent evidence implicates hs-CRP, and thus inflammation, in the metabolic syndrome and diabetes mellitus, particularly in women. As a clinical tool for cardiovascular risk assessment, hs-CRP testing enhances information provided by lipid screening or global risk assessment. Statin therapy and other interventions can lower hs-CRP. Whether or not such reductions can prevent cardiovascular events is under investigation.

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Inflammatory Diseases and Vitamin E—What Do We Know and Where Do We Go?

Wallert

Börmel

Lorkowski

2020

Molecular Nutrition Food Res

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Inflammation‐driven diseases and related comorbidities, such as the metabolic syndrome, obesity, fatty liver disease, and cardiovascular diseases cause significant global burden. There is a growing body of evidence that nutrients alter inflammatory responses and can therefore make a decisive contribution to the treatment of these diseases. Recently, the inflammasome, a cytosolic multiprotein complex, has been identified as a key player in inflammation and the development of various inflammation‐mediated disorders, with nucleotide‐binding domain and leucine‐rich repeat pyrin domain (NLRP) 3 being the inflammasome of interest. Here an overview about the cellular signaling pathways underlying nuclear factor “kappa‐light‐chain‐enhancer” of activated B‐cells (NF‐κB)‐ and NLRP3‐mediated inflammatory processes, and the pathogenesis of the inflammatory diseases atherosclerosis and non‐alcoholic fatty liver disease (NAFLD) is provided; next, the current state of knowledge for drug‐based and dietary‐based interventions for treating cardiovascular diseases and NAFLD is discussed. To date, one of the most important antioxidants in the human diet is vitamin E. Various in vitro and in vivo studies suggest that the different forms of vitamin E and also their derivatives have anti‐inflammatory activity. Recent publications suggest that vitamin E—and possibly metabolites of vitamin E—are a promising therapeutic approach for treating inflammatory diseases such as NAFLD.

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C-reactive protein: The pawn has been promoted to queen

Cited by 30 publications

References 59 publications

Inflammatory Cytokines Stimulated C-Reactive Protein Production by Human Coronary Artery Smooth Muscle Cells

Inflammatory Cytokines Stimulated C-Reactive Protein Production by Human Coronary Artery Smooth Muscle Cells

High-sensitivity C-reactive protein as a risk assessment tool for cardiovascular disease

Inflammatory Diseases and Vitamin E—What Do We Know and Where Do We Go?

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