Objective— Atherosclerotic blood vessels overexpress connective tissue growth factor E-mail [email protected] . Sakai N, Yamashita S, Matsuzawa Y, Nojima N. Large scale isolation of non-uniform shear . () Carotid Plaque Vulnerability, Stroke, , (), Online publication date: 1-Dec However, the risks for mortality and atherosclerotic complications in incident HD patients E-mail: [email protected] . procedure codes, health care costs, dates of admission and discharge, death dates, outpatient and .. Liu Y, Coresh J, Eustace JA, Longenecker JC, Jaar B, Fink NE, et al. mail: [email protected] Received date: November 29, ; Accepted date: January 2, ; Published date: January 10, Copyright: © development of atherosclerotic lesions involves a chronic inflammatory response .. Mahajan N, Malik N, Bahl A, Sharma Y, Dhawan V () Correlation.
Results showed that serum levels of SPD were On the other hand, the SPM levels were These results demonstrated that SPD and SPM levels were altered in sera of atherosclerosis patients when compared with the control group. Generally, correlations were observed among the SPD and SPM levels, the white blood cell differential, and the red blood cells in the sera of atherosclerosis patients.
Copy the following to cite this article: Biomed Pharmacol J ;11 3. Copy the following to cite this URL: It constricts and reduces blood flow within the artery leading to the heart muscle especially when fatty substances accumulate on the inner wall of the coronary arteries.
Atherosclerosis is considered the major cause of morbidity and mortality in industrialized countries. Therefore, the purpose of this study is to measure the concentrations of SPD and SPM in the sera of Iraqi patients with atherosclerosis and their correlation with this disease and white blood cell count, in addition to the difference of gender on polyamine concentration.
Materials and Methods Study Subjects A total of patients suffering from atherosclerosis symptoms were enrolled in this study. Collection of Blood Samples A volume of 7 ml of blood samples was collected from each case study and divided to two parts. The remaining blood was placed in plain tubes and left to stand for 10 minutes at room temperature until clot formation.
These tubes were then centrifuged at rpm for 10 minutes. High serum levels of resistin were not only found to correlate positively with established surrogate markers of atherosclerosis development and progression, including coronary artery calcification [ 2122 ], but they also predicted the occurrence of major adverse cardiovascular events. The prognostic value of resistin as an independent predictor of cardiovascular events, including myocardial infarction, extended both to patients with stable coronary artery disease [ 2324 ] and to healthy primary prevention populations [ 25 ].
Moreover, in patients with more severe ASCVD, including those with acute coronary syndrome and individuals with atherothrombotic ischemic stroke, elevated resistin was independently associated with a poor prognosis, including the occurrence of future cardiovascular events and increased mortality [ 2627 ].
Adverse Effects of Resistin at the Arterial Wall The finding that resistin immunoreactivity is increased in atherosclerotic regions of the human vasculature [ 28 ] seemed to indicate that at least part of the mechanism of action of resistin in promoting ASCVD involved stimulation of the atherosclerosis process directly at the arterial wall.Causes Symptoms and Treatment of Atherosclerosis
Consistent with this, studies have shown that resistin is involved in pathophysiological pro-atherogenic processes in multiple cell types in the arterial wall. More specifically, resistin has been found to promote endothelial cell dysfunctionsmooth muscle cell migration and proliferation and monocyte and macrophage activation and transformation.
To begin with, in several different cell systems, including human coronary artery endothelial cells, resistin has been reported to induce endothelial dysfunction, one of the earliest impairments at the vascular wall in the atherosclerosis process. Resistin was shown to mediate endothelial cell dysfunction via downregulation of cellular eNOS mRNA and protein levels [ 29 ].
Resistin, thereby, potentially impairs endothelial-dependent vasorelaxation. The mechanisms through which resistin mediates a reduction in endothelial cell eNOS levels in humans is not known but has been investigated in other species, including in porcine and rodent endothelial cells.
Next, resistin has been found to induce aberrant activity of human vascular smooth muscle cells.
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In addition, resistin was shown to stimulate the pro-atherogenic vessel process of vascular smooth muscle cell migration [ 3132 ].
Finally, resistin has been shown to have pathophysiological effects on human monocytes and macrophages. The migration and recruitment of circulating monocytes and macrophages into the subendothelial space is a critical component of the initiation of the chronic inflammatory component of atherosclerosis [ 33 ]. Furthermore, increased monocyte adhesion to endothelial cells by resistin was dependent on resistinmediated increases in endothelial cell ICAM-1 and VCAM-1 levels [ 3435 ].
Resistin has been further shown to promote monocyte and macrophage morphological transformation into lipid-filled foam cells, which constitute the major cellular component of the fatty streaks characteristic of atherosclerotic plaques. Resistin-induced transformation of human monocytes and macrophages into lipidabundant foam cells was through the upregulation of the macrophage CD36 and SR-A receptors and a consequent increase in cellular uptake of oxidized LDL particles [ 3738 ].
Resistin further downregulated macrophage expression of the ABCA1 transporter, the rate-limiting protein in cellular cholesterol efflux [ 38 ], potentially enhancing macrophage retention of intracellular cholesterol. In vivo, resistin gene transfer into atherosclerotic plaques of rabbits increased the macrophage and lipid contents of their plaques, and because of these effects, increased not only atherosclerotic plaque size and progression, but also plaque destabilization and vulnerability [ 39 ].
If the same effect of resistin in inducing atherosclerotic plaque instability holds true in humans, once tested, it would explain the increase in cardiovascular eventsincluding myocardial infarction and the poor prognosis observed in patients with elevated serum resistin levels. Overall, it should be noted that the above vascular cell proatherosclerotic effects of resistin, while broad, have only been demonstrated in humans at the in vitro level in cell culture.
A direct causal effect of resistin in promoting the development and advancement of the atherosclerosis process in the human vasculature has not been shown. Nonetheless, in light of the strong association between elevated resistin and clinical ASCVD outcomes, the question then remained if resistin mediates direct pro-atherogenic effects in humans through its actions outside the vasculature to increase ASCVD risk factors in obesity. One of the earliest metabolic defects to appear in obese individuals, which is central to the pathway of ASCVD is, dyslipidemia [ 4041 ].
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The characteristic dyslipidemia of obesity is the atherogenic dyslipidemia, which is a triad of lipoprotein disorders including: We recently identified a novel role of resistin in directly increasing the levels of the pro-atherogenic lipid and lipoprotein components of the atherogenic dyslipidemia in humans — that is, elevated triglycerides and increased LDL particle concentration [ 4445 ].
In terms of serum triglycerides, a recent large population-based Framingham study found a highly significant positive association between circulating resistin levels and serum triglycerides [ 46 ]. No studies, however had investigated whether the association between resistin and triglycerides in humans was a cause-and-effect relationship until our recent studies on the topic.
The major carrier of triglycerides in human serum is the circulating triglyceride-rich Very-Low Density Lipoprotein VLDL particles, which is, thereby, a key determinant of serum triglyceride levels.
We therefore initially wished to determine if resistin plays a role in liver VLDL production in a human setting. We found an extremely potent effect of resistin treatment in directly stimulating VLDL production by human liver hepatocytes [ 44 ]. At physiological levels of resistin characteristic of human obesity, recombinant human resistin induced a highly significant fold increase in human hepatocyte VLDL production.
The physiological relevance of the findings were further established by the demonstration that treatment of the hepatocytes with serum from obese humans with elevated resistin levels caused a greater stimulatory effect on VLDL production than serum from lean individuals with lower resistin levels.
We then determined the quantitative importance of the resistin effect in human serum in inducing VLDL production. This was shown by the substantial reduction of the stimulatory effect of obese and lean human serum on hepatocyte VLDL production when resistin was specifically removed from the serum via antibody immunoprecipitation prior to serum stimulation of the hepatocytes.
We thereafter examined the mechanisms through which human resistin induced hepatocyte VLDL overproduction [ 44 ] and found that resistin induced a stimulatory effect on the hepatic synthesis of both the major protein and lipid components of VLDL particles — apolipoprotein B apoB and triglycerides and cholesteryl esters, respectively. Finally, resistin downregulated the expression and activity of several key proteins in the insulin signalling pathway, a pathway which when activated, reduces hepatic VLDL production.
Overall, resistin mediated its potent enhancement on VLDL production in a human setting both by increasing the stimulatory signals on VLDL production and decreasing the inhibitory signals, thereby inducing a synergistic effect on VLDL production.
In this way, resistin elevates serum triglycerides in humans. Our next objective was to investigate if resistin plays a role in generating the other pro-atherogenic component of the atherogenic dyslipidemia in humans — increased LDL particle concentration [ 45 ].
However, the primary determinant of LDL levels in humans is the rate of LDL particle uptake and clearance by the liver. The rate of liver LDL uptake and clearance is, moreover, regulated primarily by hepatocyte cell surface LDL receptors. We, therefore, wished to investigate if resistin affects human hepatocyte LDL receptor regulation. The effect of resistin in reducing LDL receptor expression was dose-responsive and occurred in both cultured human HepG2 hepatocytes and primary hepatocytes freshly isolated from human livers.
The resistin-mediated decrease in LDL receptor levels was seen both when the hepatocytes were treated with recombinant human resistin and with obese human serum with elevated resistin levels.
Thus, the results were applicable physiologically to humans. At present, LDL receptor concentrations are thought to be regulated essentially by a dual mechanism. On the opposite end, PCSK9, the recently discovered protein of high current interest, functions to direct intracellular degradation of the LDL receptor [ 4849 ]. Both lipoprotein particles are taken up by macrophages and other cells in the arterial wall and are well known to induce processes in the vascular wall leading to atherothrombotic plaques [ 5051 ].
In fact, elevated serum LDL is both necessary and sufficient for atherosclerosis initiation and progression [ 52 ]. Therefore, targeting these particular dyslipidemias in obesity should certainly garner large gains in ASCVD risk reduction.
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Pathogenic adipose tissue resistin secretion in obesity-induced dyslipidemia. This premise has already been tested and proved with the substantial reductions in ASCVD progression and risk achieved in randomized clinical trials with the statins [ 53 ]. Statins are the major and most successful class of drugs administered to patients with elevated LDL and lower both LDL and VLDL significantly and effectively in a large proportion of patients receiving them [ 53 - 55 ].