Human C-reactive protein induces endothelial dysfunction and uncoupling of eNOS in vivo

Hein, Travis W.; Singh, U. S.; Vásquez‐Vivar, Jeannette; Devaraj, Sridevi; Li, Kuo; Jialal, Ishwarlal

doi:10.1016/j.atherosclerosis.2009.02.002

Cited by 141 publications

(103 citation statements)

References 47 publications

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“…dothelial nitric oxide synthase (eNOS) activity. [17][18][19][20][21] In addition, CRP downregulates the number of endothelial progenitor cells and cell function in vitro. 22) The long pentraxin PTX3 shares some similarities with CRP, but differs in terms of structural domain, gene organization, cellular and tissue sources, inducing stimuli, and recognized ligands.…”

Section: Discussionmentioning

confidence: 99%

Plasma Pentraxin 3 is a More Potent Predictor of Endothelial Dysfunction than High-Sensitive C-Reactive Protein

et al. 2014

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SummaryAn infl ammatory response is a key event for endothelial dysfunction. Pentraxin 3 (PTX3) is an infl ammatory protein produced at infl ammation sites such as leukocytes and vascular endothelial cells. Here, we compared the relationships between endothelial function assessed by fl ow-mediated dilation (FMD), and the levels of plasma PTX3 and highsensitive C-reactive protein (hsCRP), another infl ammatory protein of the pentraxin family.Levels of FMD, PTX3 and hsCRP were measured twice within 6 to 8 months and retrospectively analyzed in 36 patients with coronary artery disease. We examined the associations between the values of FMD and the levels of PTX3 and hsCRP at the fi rst measurement, and between the change ratios (second value/fi rst value) of these parameters.Univariate linear regression analysis showed signifi cantly negative correlations between FMD values and PTX3 and hsCRP levels at the fi rst measurement, and signifi cant associations with taking statins or calcium antagonists. Multivariate linear stepwise regression analysis identifi ed PTX3 levels and taking statins and calcium antagonists as independent factors for endothelial function. The change ratio of FMD correlated more closely with that of PTX3 than of hsCRP (r = -0.446, P = 0.006 versus r = -0.330, P = 0.050). Signifi cantly more patients with decreased FMD values had increased levels of PTX3 than those of hsCRP at the second measurement compared with the fi rst measurement. Furthermore, the ratio of patients with increased PTX3, but not increased hsCRP, was signifi cantly reduced among those with increased, rather than decreased, FMD values.Endothelial dysfunction might be more accurately predicted by plasma PTX3 levels than by serum hsCRP levels. (Int Heart J 2014; 55: 160-164)

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Section: Discussionmentioning

confidence: 99%

Plasma Pentraxin 3 is a More Potent Predictor of Endothelial Dysfunction than High-Sensitive C-Reactive Protein

et al. 2014

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“…HMGA1 has been extensively studied as a transforming factor linking viral infection and other perturbations to cancer (reviewed in Reference 35) and HMGA1 is also highly proinflammatory in ECs in response to viral infection (36). The increase in NOS3 expression may reflect uncoupling of NO and peroxynitrite production seen with elevated thromboxane (37) and with inflammation (38). Up-regulation of the NOS3 transcript may represent an attempt to make up for reduced levels of the NOS3 protein in PAH as has been recently shown (39).…”

Section: Discussionmentioning

confidence: 99%

RNA Sequencing Analysis Detection of a Novel Pathway of Endothelial Dysfunction in Pulmonary Arterial Hypertension

Rhodes

Cao

et al. 2015

Am J Respir Crit Care Med

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Rationale: Pulmonary arterial hypertension is characterized by endothelial dysregulation, but global changes in gene expression have not been related to perturbations in function.Objectives: RNA sequencing was used to discriminate changes in transcriptomes of endothelial cells cultured from lungs of patients with idiopathic pulmonary arterial hypertension versus control subjects and to assess the functional significance of major differentially expressed transcripts.Methods: The endothelial transcriptomes from the lungs of seven control subjects and six patients with idiopathic pulmonary arterial hypertension were analyzed. Differentially expressed genes were related to bone morphogenetic protein type 2 receptor (BMPR2) signaling. Those down-regulated were assessed for function in cultured cells and in a transgenic mouse.Measurements and Main Results: Fold differences in 10 genes were significant (P , 0.05), four increased and six decreased in patients versus control subjects. No patient was mutant for BMPR2. However, knockdown of BMPR2 by siRNA in control pulmonary arterial endothelial cells recapitulated 6 of 10 patient-related gene changes, including decreased collagen IV (COL4A1, COL4A2) and ephrinA1 (EFNA1). Reduction of BMPR2-regulated transcripts was related to decreased b-catenin. Reducing COL4A1, COL4A2, and EFNA1 by siRNA inhibited pulmonary endothelial adhesion, migration, and tube formation. In mice null for the EFNA1 receptor, EphA2, versus control animals, vascular endothelial growth factor receptor blockade and hypoxia caused more severe pulmonary hypertension, judged by elevated right ventricular systolic pressure, right ventricular hypertrophy, and loss of small arteries. Conclusions:The novel relationship between BMPR2 dysfunction and reduced expression of endothelial COL4 and EFNA1 may underlie vulnerability to injury in pulmonary arterial hypertension.

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“…Since by searching the literature we could not find similar study we could not compare our results with results of other authors. Possible explanation for obtained results might be proven effect of CRP on inhibition of eNOS in experimental studies (Singh et al 2007, Hein et al 2009). Results of these studies have shown that CRP inhibits GTP cyclohydrolase 1 and stimulates NADPH oxidase which induces decrease of tetrahydrobiopterin and increase of reactive oxygen species resulting in decreased activity of eNOS and consequently decreased bioavailability of NO.…”

Section: Resultsmentioning

confidence: 99%

Elevated Serum C-Reactive Protein Level Is Not Associated With Serum Nitric Oxide in Patients With Posttraumatic Stress Disorder

et al. 2017

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SUMMARYBackground: The aim of the present study was to evaluate serum nitric oxide (NO) PTSD (r=0.118; p=0.727 mg/L). Serum NO concentration in veterans with (7.64±4.43 µmol/L) and without PTSD (7.12±2.60 µmol/L) was significantly lower (p<0.05) compared to control group (11.26±7.01 µmol/L). Statistically significant correlation between serum NO and CRP concentration was determined in veterans without PTSD (r=-0.473; p<0.01). No correlation was observed between serum NO and CRP concentration in veterans with

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Human C-reactive protein induces endothelial dysfunction and uncoupling of eNOS in vivo

Cited by 141 publications

References 47 publications

Plasma Pentraxin 3 is a More Potent Predictor of Endothelial Dysfunction than High-Sensitive C-Reactive Protein

Plasma Pentraxin 3 is a More Potent Predictor of Endothelial Dysfunction than High-Sensitive C-Reactive Protein

RNA Sequencing Analysis Detection of a Novel Pathway of Endothelial Dysfunction in Pulmonary Arterial Hypertension

Elevated Serum C-Reactive Protein Level Is Not Associated With Serum Nitric Oxide in Patients With Posttraumatic Stress Disorder

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