Platelet activation is associated with hypoadiponectinemia and carotid atherosclerosis

Shoji, Takuhito; Koyama, Hidenori; Fukumoto, Shinya; Maeno, Takaaki; Yokoyama, Hisayo; Shinohara, K.; Emoto, Masanori; Shoji, Tetsuo; Yamane, Takahisa; Hino, Masayuki; Shioi, Atsushi; Nishizawà, Yoshiki

doi:10.1016/j.atherosclerosis.2005.10.034

Cited by 44 publications

(35 citation statements)

References 30 publications

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“…The fact that both parameters increase in patients with hypercholesterolemia and atherosclerosis, that is, the fact that patients are at a risk for an ischemic event, suggests that platelet activation and aggregation are involved in the pathogenesis of stroke [6,7,8]. Activated platelets recruit monocytes to the vessel wall and facilitate penetration into the subendothelial space, where monocytes differentiate into macrophages and contribute to the development of atherosclerosis [9].…”

Section: Introductionmentioning

confidence: 99%

Determinants of Platelet-Leukocyte Aggregation and Platelet Activation in Stroke

Schmalbach¹,

Stepanow²,

Jochens

et al. 2015

Cerebrovasc Dis

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Background: Platelet-leukocyte aggregation (PLA) and platelet activation are found to be on the higher side in ischemic stroke patients. The correlation of PLA with clinical features has not been intensively investigated and the influence of genetic factors on PLA is still unexplored. The interaction of platelets with leukocytes is mainly determined by the proteins encoded by six genes: P-Selectin (SELP encodes CD62P) on the thrombocyte binding to P-Selectin-Glycoprotein-Ligand-1 (PSGL1) on the leukocyte, intracellular-adhesion-molecule 2 (ICAM2) interacting with Integrin alpha M (ITGAM) and Glycoprotein 1b-alpha (GP1BA) binding to Integrin alpha L (ITGAL). Methods: Seventy-nine patients with acute ischemic stroke and 151 controls without vascular disease from a single German center were enrolled. A neurologist and a neuroradiologist ascertained clinical and radiological features. PLA and platelet activation were analyzed using flow cytometry with various antibodies. Coding as well as tagging SNPs in six genes determining PLA were genotyped. Three groups of parameters were correlated with each other: (i) clinical and radiological parameters, (ii) laboratory parameters, (iii) genetic parameters. For the comparisons, robust nonparametric statistical tests were applicable. Results: PLA and platelet activation were higher in ischemic stroke patients compared to controls. Both, anticoagulant and antiplatelet treatment in the patient group affected platelet activation but not PLA. PLA correlated weakly with measures of stroke severity but not with thrombus length or stroke etiology. The association of SNP rs2228315 in the P-Selectin Glycoprotein Ligand-1-gene (PSGL1) with ischemic stroke and platelet activation was significant before correction for multiple testing while a trend was observed for the association with PLA. Regression analysis revealed that (i) platelet activation was an independent determinant of stroke, (ii) that PLA correlated with stroke, sex, age and platelet activation and (iii) that platelet activation correlated only with stroke. None of the SNPs survived in the regression analysis for stroke, PLA or platelet activation as dependent variables. Conclusions: The most important result of our study is that PLA and platelet activation are independent of other vascular risk factors correlated with stroke in our sample. In addition, we identified the missense SNP rs2228315 in the PSGL1-gene as a candidate polymorphism for ischemic stroke-related PLA. Association between this SNP and stroke as well as coronary artery disease has also been shown by two other studies.

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Section: Introductionmentioning

confidence: 99%

Determinants of Platelet-Leukocyte Aggregation and Platelet Activation in Stroke

Schmalbach¹,

Stepanow²,

Jochens

et al. 2015

Cerebrovasc Dis

View full text Add to dashboard Cite

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“…Platelet surface P-selectin was analyzed by whole-blood flow cytometry essentially as described previously 24) . Platelet-monocyte binding was measured by flow cytometry as described previously 25) .…”

Section: Platelet Activation Measurementmentioning

confidence: 99%

Comparison of the Effect of Cilostazol with Aspirin on Circulating Endothelial Progenitor Cells and Small-Dense LDL Cholesterol in Diabetic Patients with Cerebral Ischemia: A Randomized Controlled Pilot Trial

Ueno

Koyama

Mima

et al. 2011

JAT

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Aim:A recent clinical trial showed the preventive effect of cilostazol on cerebrovascular diseases. We compared the effects of cilostazol with aspirin on circulating endothelial progenitor cells (EPCs), a surrogate marker for cardiovascular disease, and lipid metabolism in a randomized controlled trial (UMIN000000537). Methods: Forty-nine diabetic outpatients with leukoaraiosis or asymptomatic old cerebral infarction were enrolled in the study with written informed consent. They were randomly assigned to a cilostazol (200 mg daily, n 24) or aspirin group (100 mg daily, n 25), and followed for 16 weeks. Changes in circulating CD34 CD45 low CD133 VEGFR2 EPCs ( EPC) were a primary endpoint. Changes in CD34 CD45 low CD133 progenitor cells ( PC), p-selectin-positive platelet, plateletmonocyte binding measured by flow cytometry, LDL-, HDL-, small dense LDL (sdLDL)-cholesterol and triacylglycerol were the secondary endpoints. Results: Twenty patients in each group completed the study. EPC were significantly higher in the cilostazol group than aspirin group at 16 weeks, while PC were already significantly higher at 4 weeks in the cilostazol group. Changes in p-selectin-positive platelets and platelet-monocyte binding were similar in both groups. The cilostazol group showed significantly less sdLDL-and higher HDLcholesterol than the aspirin group at both 4 and 16 weeks. EPC were significantly and inversely correlated with changes of sdLDL, while positively with those of HDL. Analysis of covariance showed that a significant relation of EPCs with cilostazol treatment was confounded by changes in HDL-and sdLDL-cholesterol. Conclusion: Cilostazol increases circulating EPCs and decreases small-dense LDL in diabetic patients with cerebral ischemia. J Atheroscler Thromb, 2011; 18:883-890.

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“…At lower levels, adiponectin induces a proinfl ammatory state [ 35 , 36 ]. In addition, low levels of adiponectin have been recently reported to be associated with platelet aggregation [ 37 ]. Leptin and resistin are two other substances secreted by the adipocytes that may be of importance.…”

Section: Secreted By the Adipose Tissuementioning

confidence: 99%

“…Beyond their effects on central metabolic functions, leptin, resistin, and adiponectin have profound effects on a number of other physiologic processes, including infl ammation [ 36 ]. It has been demonstrated that leptin and adiponectin activate proinfl ammatory cytokine release and phospholipid metabolism in the adipose tissue, and that anti-infl ammatory agents counteract the induced infl ammation [ 37 ]. The underlying mechanisms seem to involve a nitric oxide-dependent pathway [ 37 ].…”

Section: Secreted By the Adipose Tissuementioning

confidence: 99%

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Putative mechanisms of the relationship between obesity and migraine progression

Bigal

Lipton²

2008

Current Science Inc

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Studies suggest that obesity is associated with migraine progression from an episodic into a chronic form. We discuss putative mechanisms to justify this relationship. Several of the inflammatory mediators that are increased in obese individuals are important in migraine pathophysiology, including interleukins and calcitonin gene-related peptide. Both migraine and obesity are prothrombotic states. Substances that are important in metabolic control are nociceptive at certain levels. Hypothalamic dysfunction in the orexin pathways seems to be a risk factor for both conditions. In addition, we discuss the importance of metabolic syndrome and autonomic dysfunction in modulating the obesity/migraine progression relationship.

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Platelet activation is associated with hypoadiponectinemia and carotid atherosclerosis

Cited by 44 publications

References 30 publications

Determinants of Platelet-Leukocyte Aggregation and Platelet Activation in Stroke

Determinants of Platelet-Leukocyte Aggregation and Platelet Activation in Stroke

Comparison of the Effect of Cilostazol with Aspirin on Circulating Endothelial Progenitor Cells and Small-Dense LDL Cholesterol in Diabetic Patients with Cerebral Ischemia: A Randomized Controlled Pilot Trial

Putative mechanisms of the relationship between obesity and migraine progression

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