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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inflammation plays a pivotal role in atherosclerosis. In addition to being a risk marker for cardiovascular disease, much recent data support a role for C-reactive protein (CRP) in atherogenesis. Interleukin-8 (IL-8), a member of the CXC chemokines promotes monocyte-endothelial cell adhesion and arrest and is abundant in atherosclerotic plaques. However, there is a paucity of data examining the effect of CRP on IL-8 secretion in human aortic endothelial cells (HAEC). In this report, we show that incubation of HAEC with CRP resulted in a time and dose-dependent increase in IL-8 protein and mRNA via transcription. In contrast to human umbilical vein endothelial cells, monocyte-chemoattractant protein-1 expression in HAEC was not affected by CRP. Furthermore, CRP upregulated NF-kappa B activity in HAEC and inhibitors of NF-kappa B significantly reversed the upregulation of IL-8 by CRP. Blocking antibodies to IL-8 significantly decreased monocyte-endothelial cell adhesion induced by CRP (31%, P<0.01). In conclusion, this study makes the novel observation that CRP induces IL-8 synthesis and secretion in HAEC via upregulation of NF-kappa B activity.
J Mol Cell Cardiol 2004 Mar
PMID:Effect of C-reactive protein on chemokine expression in human aortic endothelial cells. 1501 Feb 79

C-reactive protein (CRP) and surfactant protein A (SP-A) are phosphatidylcholine (PC) binding proteins that function in the innate host defense system. We examined the effects of CRP and SP-A on the surface activity of bovine lipid extract surfactant (BLES), a clinically applied modified natural surfactant. CRP inhibited BLES adsorption to form a surface-active film and the film's ability to lower surface tension (gamma) to low values near 0 mN/m during surface area reduction. The inhibitory effects of CRP were reversed by phosphorylcholine, a water-soluble CRP ligand. SP-A enhanced BLES adsorption and its ability to lower gamma to low values. Small amounts of SP-A blocked the inhibitory effects of CRP. Electron microscopy showed CRP has little effect on the lipid structure of BLES. SP-A altered BLES multilamellar vesicular structure by generating large, loose bilayer structures that were separated by a fuzzy amorphous material, likely SP-A. These studies indicate that although SP-A and CRP both bind PC, there is a difference in the manner in which they interact with surface films.
Am J Physiol Lung Cell Mol Physiol 2004 Dec
PMID:Disparate effects of two phosphatidylcholine binding proteins, C-reactive protein and surfactant protein A, on pulmonary surfactant structure and function. 1531 May 57

Cerebral ischemia triggers interleukin-6 (IL-6) release into blood. IL-6 is a key mediator of acute phase reaction. Markers of acute phase reaction (C-reactive protein, fibrinogen, fever) have been linked to poor prognosis in stroke patients. Interleukin-6 soluble receptor (sIL-6R) can potentiate IL-6 pro-inflammatory activity. The aim of this study was to investigate the relationship between IL-6 and sIL-6R in stroke patients. Serum cytokine levels were measured in 18 stroke patients and 13 controls using the ELISA method. On the second day of stroke, IL-6 levels were significantly higher in stroke patients than in controls; sIL-6R levels did not differ significantly between groups. Three months after stroke, IL-6 levels did not differ significantly between groups; sIL-6R levels were significantly decreased in stroke patients when compared with that in controls and with levels in acute phase of stroke. Decreased sIL-6R early after stroke might reflect a regulatory mechanism attenuating inflammatory response.
J Mol Neurosci 2004
PMID:Serum interleukin-6 soluble receptor in relation to interleukin-6 in stroke patients. 1545 42

The aim of this study was to monitor the ontogenic development of innate immune parameters of cod (Gadus morhua L.) and to determine the presence of maternal IgM. The general protein composition and enzyme activity was also studied. At intervals, samples were collected of fertilized cod eggs and larvae from 3 days after fertilization until 57 days after hatching. Cell lysates were prepared and analysed by Western blotting using antibodies prepared against cod IgM, the complement component C3 and C-reactive protein (CRP) as well as against cod serum proteins and haemoglobin. Antibodies against salmon cathepsins and against several mammalian proteins of immunological significance were also used. Maternal IgM was not detected but C3 and the closely associated apolipoprotein A-I were present from the time of embryo organogenesis. C-reactive protein was not detected and none of the antibodies against mammalian immune parameters cross-reacted with the cod material. Protein and proteomic analysis showed that the major proteins of the egg samples were vitellogenin derived maternal proteins. Other non-vitellogenin maternal proteins, not yet identified, were also detected in the fertilized eggs. Cathepsin was present in all samples, but other enzyme activity was restricted to larval samples from 4 days after hatching when feeding had commenced. Haemoglobin was not detected until 10 days after hatching.
Comp Biochem Physiol B Biochem Mol Biol 2004 Oct
PMID:The ontogenic development of innate immune parameters of cod (Gadus morhua L.). 1546 68

Serum C-reactive protein (CRP) has been strongly implicated in the pathogenesis of coronary heart disease (CHD). We report here on the association between gene coding for CRP and CHD in the ethnic Han population of China. For this purpose two polymorphisms of -717A>G and +2147A>G of the CRP gene were identified by direct sequencing of genomic DNA derived from 48 randomly selected patients and these were further investigated for associations with CHD in 619 male patients and 615 age-matched male normal controls. The frequency of A allele carriers of -717A>G polymorphism was significantly higher in patients than in controls by univariate analysis. After controlling for other risk factors the association between this polymorphism and CHD remained significant by multivariate logistic regression analysis. Individuals carrying the -717A allele had an approx. 6.8-fold higher risk of developing CHD (odds ratio 6.84 compared with those not carrying this allele). Haplotype analysis confirmed the results of individual polymorphism analyses. However, the resolution of effect size is poor, which may be due to the deficiency in sample size of this study. Neither polymorphism was observed to have an influence on serum CRP level. Since the frequency difference between CHD cases and controls for the -717A allele carriers is only 2.28%, and homozygosity for -717G occurs in only 1.78% of subjects, -717 A>G polymorphism is not a major determinant of population genetic risk of CHD in the Chinese population. The association of this polymorphism with CHD supports the belief that carriers of -717A allele of the CRP gene are genetically predisposed to CHD in the Chinese Han population, and it remains possible that this polymorphism is in disequilibrium with one as yet unidentified functional polymorphism in the vicinity.
J Mol Med (Berl) 2005 Jan
PMID:-717A>G polymorphism of human C-reactive protein gene associated with coronary heart disease in ethnic Han Chinese: the Beijing atherosclerosis study. 1551 31

An active role for C-reactive protein (CRP) in inflammatory vascular diseases has been recently suggested. Monocytes play an important role in vascular pathology and are activated by p38 mitogen activated protein kinase (MAPK) dependent mechanisms in many inflammatory settings. Therefore, we investigated whether CRP directly promotes a pro-inflammatory phenotype in human peripheral blood mononuclear cells (HPBMC) via p38 MAPK signaling. CRP exposure leads to a rapid phosphorylation of p38 MAPK in HPBMC. CRP-induced p38 kinase activity in HPBMC was blocked by treatment with an inhibitor of p38 kinase, SD-282. CRP-induced the expression of tissue factor protein and the secretion of IL-6, IL-8, IL-1beta, TNFalpha and PGE(2). Co-exposure to CRP and SD-282 blocked the secretion of these pro-inflammatory and pro-thrombotic mediators. CRP treatment elevated IL-6, IL-8, IL-1beta, TNFalpha, COX-2 and TF mRNA expression. These effects of CRP also required p38 activity, since SD-282 blocked mRNA induction of each. Taken together these data suggest a mechanistic relationship between p38 MAPK signaling and CRP-induced pro-inflammatory and pro-thrombotic activities in HPBMC. Thus, p38 inhibition may represent a novel approach to attenuate inflammation and its consequences in cardiovascular disease.
J Mol Cell Cardiol 2004 Dec
PMID:p38 Inhibition attenuates the pro-inflammatory response to C-reactive protein by human peripheral blood mononuclear cells. 1557 41

Patients with Gaucher disease, perhaps due to chronic storage of glycolipids, apparently harbor a subclinical or underlying inflammation. Quantification of a baseline inflammatory profile in patients with Gaucher disease is more impressive when compared with that of matched healthy controls in a systematic, automated fashion. A mean of 16 healthy controls was generated for each of 50 patients with Gaucher disease by applying variables relating to potential for inflammatory features, for example, atherothrombotic risk factors. Relative to matched controls, male patients with Gaucher disease had significant elevations in fibrinogen (312 +/- 61 vs. 244 +/- 21 mg/dl; P = 0.002), accelerated erythrocyte sedimentation rate (ESR) (21.5 +/- 16.1 vs. 7.0 +/- 1.4 mm/H; P = 0.004), and elevated high-sensitivity C-reactive protein (hs-CRP) (1.4 +/- 2.4 vs. 0.9 +/- 1.6 mg/l; P = 0.026). Comparison of female patients versus controls revealed significant elevations in fibrinogen (337 +/- 81 vs. 273 +/- 19 mg/dl; P < 0.0005) and accelerated erythrocyte sedimentation rate (33.1 +/- 22.2 vs. 15.6 +/- 3.1 mm/H; P < 0.0005). Enzyme replacement therapy for Gaucher disease did not affect these values. Comparison with the matched healthy controls highlights the true low-grade inflammatory profile in Gaucher disease. By employing information from well-matched controls, even low-grade inflammatory conditions that may have otherwise been considered "within normal limits" can be teased out. This approach is not disease-specific and can be easily applied to any acute or subacute inflammatory disease/condition.
Blood Cells Mol Dis
PMID:Automated system to detect low-grade underlying inflammatory profile: Gaucher disease as a model. 1560 96

In vivo models of myocardial infarction induced by coronary artery ligation (CAL) in rats usually suffer from high early mortality and a low rate of induction. This study investigated the time course initiation of chronic myocardial infarction (CMI) in albino rats and the possibility of reducing early mortality rate due to myocardial infarction by modification of the surgical technique. CAL was carried out by passing the suture through the epicardial layer around the midway of the left anterior descending coronary artery including a small area of the myocardium to avoid mechanical damage to the heart geometry. In addition, the role of endothelin-1 (ET-1) in rat heart with congestive heart failure was critically assessed. Time course initiation experiments were designed by sacrificing the animals at different time intervals and by carrying out physiological, biochemical, histopathological, electron microscopical and immunohistochemical studies. Specific markers of myocardial injury, viz. cardiac troponin-T (cTnT), high sensitivity C-reactive protein, lactate dehydrogenase and fibrinogen were measured at different time points. Serum marker enzymes and activities of lysosomal hydrolases were found to be elevated on the eighth day post-ligation. Histopathological studies demonstrated focal areas showing fibrovascular tissue containing fibroblasts, collagenous ground substance and numerous small capillaries replacing cardiac muscle fibers. Transmission electron micrographs exhibited mitochondrial changes of well-developed irreversible cardiac injury, viz. swelling, disorganization of cristae, appearance of mitochondrial amorphous matrix densities, significant distortion of muscle fibers and distinct disruption of the intercalated discs. Immunoblotting studies confirmed the presence of alpha 2-macroglobulin which supported the inflammatory response. The severity of the CMI was inferred by the measurement of the level of ET-1 in plasma and left ventricle which was significantly higher in the CMI rats than in the sham-operated rats. Immunohistochemical studies at different time intervals showed that there was a significant immunoexpression of ET-1 on the eighth day post-ligation. This study conclusively showed that ligation of left anterior descending artery minimized mortality and ET-1 was expressed during CMI.
Mol Cell Biochem 2004 Dec
PMID:Time course studies on the functional evaluation of experimental chronic myocardial infarction in rats. 1566 85

Coronary vascular disease (CVD) is a chronic, multifactorial disease that occurs often in individuals without known risk factors. We investigated the predictive value of homocysteine (Hcy) in relation to C-reactive protein (CRP) and low-density lipoprotein (LDL)-cholesterol in patients with confirmed coronary disease. The study included 87 German and 92 Syrian patients in addition to 87 German and 64 Syrian control individuals. Patients and controls were of comparable age, lifestyles and cultural background. Patients of both ethnic groups had significantly higher concentrations of Hcy and C-reactive protein compared to the controls. The lipids were higher only in Syrian patients compared to the controls. Elevated concentrations of Hcy or that of CRP (>75th percentiles) were associated with increased probability for CVD. In both population groups, the risk increased markedly in subjects who had elevated concentrations of Hcy and CRP or those who had elevated concentrations of Hcy and LDL-cholesterol. The results emphasize that detemination of Hcy may improve the predictive value of C-reactive protein and the LDL-cholesterol. Measurements of these markers are especially important for identification of patients at high risk for CVD.
Cell Mol Biol (Noisy-le-grand) 2004 Dec
PMID:Homocysteine in relation to C-reactive protein and low-density lipoprotein cholesterol in assessment of cardiovascular risk. 1570 53

The purpose of this study was to determine whether benign hereditary leukopenia-neutropenia in Yemenites may be reflective of an absent or a lesser degree of chronic low grade inflammation that has been documented to exist in most apparently healthy subjects. The white blood cell count (WBCC), fibrinogen as well as high sensitivity C-reactive protein (hs-CRP) concentrations were determined in a group of apparently healthy individuals during their routine health screening program. These inflammatory biomarkers in a group of 82 Yemenite Jews were compared to those measured in a group of 1817 individuals whose parents immigrated to Israel from Central and East Europe, from countries surrounding the Mediterranean Sea as well as the Middle East. The two study groups were matched for possible confounding factors that may have an influence on the intensity of the microinflammatory response including age, gender, body mass index, components of the metabolic syndrome and the Ten Year Calculated Coronary Heart Disease Framingham Risk Score. The expected reduced WBCC was noted in the group of Yemenite Jews (6.99 +/- 1.64 versus 5.88 +/- 2.06 x 10(3)/microL cells, P = 0.001). However, they had significantly enhanced concentrations of hs-CRP, the respective values being 2.1 +/- 2 versus 1.4 +/- 2.4 mg/L in men (P = 0.002) and 2.5 +/- 2.2 versus 1.4 +/- 2.9 in women (P < 0.0005). An increased concentration of fibrinogen was found in the Yemenite Jews, although the difference was not statistically significant in men. Thus, the leukopenia-neutropenia in Yemenite Jews is probably not an expression of an absent or lesser degree of chronic low grade inflammation. These findings shed more light on the potential mechanisms that are responsible for the low WBCC in this particular ethnic group.
Blood Cells Mol Dis
PMID:Benign hereditary leukopenia-neutropenia does not result from lack of low grade inflammation. A new look in the era of microinflammation. 1572 95


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