Von Willebrand Factor, Soluble P-Selectin, and Target Organ Damage in Hypertension

Spencer, Charles T.; Gurney, David; Blann, Andrew D.; Beevers, D. G.; Lip, Gregory Y.H.

doi:10.1161/01.hyp.0000022061.12297.2e

Cited by 74 publications

(50 citation statements)

References 42 publications

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“…Elevated levels of plasma VWF are related to adverse cardiovascular outcomes (36). Hypertensive patients with target organ damage are at high risk of adverse cardiovascular events, particularly myocardial infarction and stroke (37), and there is a relationship between target organ damage and endothelial damage/dysfunction in hypertension. Although the functional significance of the Val471Ile mutant remains to be determined, the mutant likely has adverse effects on the vasculature.…”

Section: Discussionmentioning

confidence: 99%

Association of Sixty-One Non-Synonymous Polymorphisms in Forty-One Hypertension Candidate Genes with Blood Pressure Variation and Hypertension

et al. 2006

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We previously selected a group of hypertension candidate genes by a key word search using the OMIM database of NCBI and validated 525 coding single nucleotide polymorphisms (SNPs) in 179 hypertension candidate genes by DNA sequencing in a Japanese population. In the present study, we examined the association between 61 non-synonymous SNPs and blood pressure variations and hypertension. We used DNA samples taken from 1,880 subjects in the Suita study, a population-based study using randomly

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Section: Discussionmentioning

confidence: 99%

Association of Sixty-One Non-Synonymous Polymorphisms in Forty-One Hypertension Candidate Genes with Blood Pressure Variation and Hypertension

et al. 2006

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“…29,30 Although the link between hemostasis and inflammation is less clear in hypertension, this disease is associated with altered platelet function. Platelets from hypertensive subjects have an increased tendency to aggregate, 31 an increased expression of P-selectin, 32,33 and increased intraplatelet calcium (a measure of cell activation). 34 Antiplatelet agents have also been shown to confer a degree of benefit to "high-risk" hypertensive patients.…”

Section: Plateletsmentioning

confidence: 99%

Modulation of the Inflammatory Response in Cardiovascular Disease

2004

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Abstract-There is a growing body of evidence that inflammation might play an important role in the initiation and progression of cardiovascular diseases (CVDs). The designation of CVD as a chronic inflammatory process is further supported by evidence that the risk factors for CVD cause endothelial cells throughout the vascular tree to assume an inflammatory phenotype. These activated endothelial cells characteristically exhibit oxidative stress and increased adhesiveness for circulating leukocytes. Although initial efforts to define the mechanisms underlying the inflammatory phenotype in diseased endothelial cells have focused on the linkage between oxidative stress and adhesion molecule activation/expression, recent work has implicated a variety of additional factors that can modulate the magnitude and/or nature of the inflammatory responses in CVD. Platelets, angiotensin II, and the CD40/CD40 ligand signaling system are gaining recognition as contributors to the pathogenesis of CVD. These factors appear to converge with known pathways that link oxidative stress with adhesion molecule expression and help to explain the apparent integration of coagulation with inflammation in CVD. These factors also hold the promise of offering multiple sites for therapeutic intervention in CVD. Key Words: oxidative stress Ⅲ integrins Ⅲ angiotensin II Ⅲ adhesion molecules I nflammation is gaining widespread attention for its role in the initiation and progression of cardiovascular disease (CVD). Epidemiological studies have revealed strong associations between biochemical markers of systemic inflammation and both the presence of and future risk for symptomatic CVD. Animal experimentation as well as clinical studies has provided convincing evidence that the known risk factors for CVD (hypertension, diabetes, hypercholesterolemia, and smoking) can elicit both an inflammatory and a prothrombogenic phenotype in the vascular system. The phenotypic changes are more pronounced in endothelial cells and can include oxidative stress, increased expression of endothelial cell adhesion molecules (CAMs), activation of cell signaling pathways (eg, the CD40/CD40 ligand [CD40L] dyad), and the consequent adhesion and activation of leukocytes and platelets. In the microcirculation, the inflammatory manifestations of CVD are more readily visible in postcapillary venules. There is growing evidence, however, that the endothelium-dependent arteriolar dysfunction often associated with CVD is also linked to the systemic inflammatory response. [1][2][3][4] Because the expression of adhesion glycoproteins by activated endothelial cells is a rate-determining step in the recruitment of inflammatory cells, much attention has been devoted to the role of endothelial CAMs in CVD. This attention has produced considerable evidence for the: (1) altered endothelial CAM expression in animal models of CVD 2,5 ; (2) use of circulating levels of soluble endothelial CAMs (eg, soluble intercellular adhesion molecule-1 [sICAM-1]) as a marker for the severity of inflammati...

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“…Earlier research documents that elevated plasma levels of VWF correspond with endothelial damage and cardiac damage. 20 VWF was upregulated in this study 1.4-fold on microarray Identification of CV genes in omentum from morbidly obese patients AK Hindle et al Identification of CV genes in omentum from morbidly obese patients AK Hindle et al Identification of CV genes in omentum from morbidly obese patients AK Hindle et al Figure 2 Genes upregulated in diabetic obese patients by microarray analysis that are involved in lipid metabolism pathways. The schematic diagram was generated with the Ingenuity pathway analysis software.…”

Section: Discussionmentioning

confidence: 58%

“…These genes are markers of CV disease and include VWF, SELP, phospholipase A2 (group VII), ANGPT1, and periostin. [20][21][22][23][24][25][26] The data revealed a statistically significant upregulation of ANGPT1 and SELP in patients with a diagnosis of hyperlipidemia versus patients with normal cholesterol levels. ANGPT1 is a member of the angiopoietin family of growth factors.…”

Section: Discussionmentioning

confidence: 86%

Identification of cardiovascular genes in omentum from morbidly obese patients with type 2 diabetes

et al. 2010

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Background: The metabolic syndrome describes the association between obesity and co-morbidities including insulin resistance, hypertension, dyslipidemia, and cardiovascular (CV) disease. Adipokines produced from omentum contribute to the risk of CV disease and increase the inflammatory state. This study examines the gene expression differences in the omental tissue of morbidly obese diabetic and non-diabetic patients. Methods: Twenty morbidly obese patients undergoing bariatric surgery were included. Ten patients were diabetic and 10 were non-diabetic. Omental samples were collected intraoperatively and snap frozen. Total RNA was extracted using the Trizol reagent and purified with the RNeasy kit (Qiagen). Microarray experiments were performed using the Affymetrix Gene 1.0 ST array and data was analyzed with the Partek 6.3 program using an unpaired t-test (Po0.05). The gene expression profiles of the diabetic group were compared with the non-diabetic group. Using the Ingenuity program, the gene list generated from the microarray analysis was evaluated and real-time quantitative PCR (qPCR) was used to validate the array data. Results: Compared with the non-diabetic group, the diabetic obese patients showed 79 upregulated genes and 4 downregulated genes with 41.4-fold difference in expression. Ingenuity analysis showed numerous dysregulated genes associated with CV disease including leptin, Von Willebrand factor, P-selectin, angiopoietin-1 (ANGPT1), phospholipase A2 (group VII), and periostin osteoblast specific factor. Microarray results for the earlier mentioned genes were confirmed with qPCR. The results were analyzed with respect to the presence or absence of hyperlipidemia, hypertension, and coronary artery disease. In patients with hyperlipidemia, ANGPT1 and P-selectin were upregulated 1.9-and 2.9-fold, respectively. Conclusions: This microarray analysis of omental tissue from morbidly obese diabetic patients documents a host of upregulated genes related to CV disease. This study provides further evidence that diabetic status predisposes obese patients to a higher risk of developing CV disease.

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Von Willebrand Factor, Soluble P-Selectin, and Target Organ Damage in Hypertension

Cited by 74 publications

References 42 publications

Association of Sixty-One Non-Synonymous Polymorphisms in Forty-One Hypertension Candidate Genes with Blood Pressure Variation and Hypertension

Association of Sixty-One Non-Synonymous Polymorphisms in Forty-One Hypertension Candidate Genes with Blood Pressure Variation and Hypertension

Modulation of the Inflammatory Response in Cardiovascular Disease

Identification of cardiovascular genes in omentum from morbidly obese patients with type 2 diabetes

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