Statin decreases endothelial microparticle release from human coronary artery endothelial cells: implication for the Rho-kinase pathway

Tramontano, Anthony F; O’Leary, Jeanne; Black, Aislinn D.; Muniyappa, Ranganath; Cutaia, Michael; El‐Sherif, Nabil

doi:10.1016/j.bbrc.2004.05.127

Cited by 123 publications

(93 citation statements)

References 22 publications

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“…While a small production of MP at the local site of plaque rupture during PCI in stable patients cannot be excluded, as we have not measured MP in the coronary sinus, it should also be considered that Inoue's patients, differently from ours, were not treated with high-dose clopidogrel and statins, which may reduce the release of MP. [30][31][32] Our study supports the accumulating evidence that MP are independent markers of increased risk of cardiovascular events in high-risk patients, 33,34 and that they are significantly higher in ACS than in SA, 7,8 raising the question of whether MP should be used as biomarkers for early prediction (or detection) of ACS as already suggested by others. 8 In our opinion, however, MP are not ready to be used as a biomarker.…”

Section: Discussionsupporting

confidence: 87%

Differences in Microparticle Release in Patients With Acute Coronary Syndrome and Stable Angina

Biasucci

Porto

Vito

et al. 2012

Circ J

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Background: Microparticles (MP) are vesicles released from activated or apoptotic cells. Endothelial MP (EMP) are derived from injured endothelium, platelet MP (PMP) from activated platelets, and Annexin V positive MP (AMP) from apoptotic endothelial cells. The aim was to assess the release of MP and its association with inflammation and atherosclerotic burden. Methods and Results:AMP, EMP and PMP were measured on admission (Day 0) in 33 patients with stable angina (SA) and 43 patients with acute coronary syndrome (ACS) undergoing percutaneous coronary interventions (PCI). In SA, peripheral artery disease (PAD) was assessed by ultrasound examination. In 30 of the 76 patients (20 ACS and 10 SA), MP, high-sensitivity-C-reactive protein (hs-CRP), and troponin T (TnT) levels were also assessed 24 h (Day 1) and 48 h (Day 2) after PCI. AMP, EMP, and PMP were higher in ACS than in SA (all P<0.01). In the SA group, AMP, PMP, and EMP were similar in patients with or without PAD. In the ACS group, AMP increased until Day 2 (P=0.001), while EMP and PMP peaked on Day 1 (P<0.01) then decreased to baseline values. Day 2 AMP correlated with Day 2 TnT levels (r=0.43, P=0.01) while Day 1 EMP and PMP correlated with Day 1 hs-CRP (r=0.37, P=0.04 and r=0.33, P=0.05; respectively). Conclusions:Higher MP levels were observed in ACS than in SA. Atherosclerotic burden did not affect MP levels in stable patients. (Circ J 2012; 76: 2174 - 2182

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Section: Discussionsupporting

confidence: 87%

Differences in Microparticle Release in Patients With Acute Coronary Syndrome and Stable Angina

Biasucci

Porto

Vito

et al. 2012

Circ J

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“…13 One study indicated fluvastatin could decrease EMP release from human coronary artery endothelial cells. 14 15 At the end of this study, the number of peripheral cEPCs was significantly elevated in the 40-mg atorvastatin group in comparison with the 10-mg atorvastatin group. A previous study suggested ICM is associated with selective impairment of progenitor cell function in the bone marrow and in the peripheral blood, which may contribute to an unfavorable LV remodeling process.…”

Section: Baseline Characteristics Of Subjects Among the 3 Groupsmentioning

confidence: 73%

Effect of 40 mg Versus 10 mg of Atorvastatin on Oxidized Low‐Density Lipoprotein, High‐Sensitivity C‐Reactive Protein, Circulating Endothelial‐Derived Microparticles, and Endothelial Progenitor Cells in Patients With Ischemic Cardiomyopathy

Huang

Cheng

Xie

et al. 2012

Clinical Cardiology

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Background: There are few recent data to delineate the beyond lipids-decreased effect of statins and the effect of different doses of statins on endothelial-derived microparticles (EMPs) and circulating endothelial progenitor cells (EPCs) in patients with ischemic cardiomyopathy (ICM). Hypothesis: Statins might have the beyond lipids-decreased effect and there were different effects between different doses of statins on EMPs and circulating EPCs in patients with ICM. Methods: One hundred patients with ICM and 100 healthy examined people, who served as the normal control group, were recruited to this study. Patients were randomly divided into 2 groups: 10-mg atorvastatin group (n = 50) and 40-mg atorvastatin group (n = 50). All subjects were followed for 1 year. The levels of serum lipids, oxidized low-density lipoprotein (oxLDL), high-sensitivity C-reactive protein (hsCRP), circulating EPCs, and EMPs were examined in all subjects. The incidences of adverse reactions in the 2 study groups were determined. Results: At the beginning of this study, there were no significant differences in baseline characteristics between the 2 study groups. At the end of this study, the levels of total cholesterol, low-density lipoprotein, serum hsCRP, oxLDL, and circulating EMPs were significantly decreased; circulating EPCs were significantly increased in the 40-mg atorvastatin group compared to the 10-mg atorvastatin group, P < 0.05. The multivariate linear regression analysis indicated that receiving only 40 mg of atorvastatin had a significant effect on the levels of circulating EPCs (β = 0.252, P = 0.014). There were no significant differences in the adverse reactions between the 2 groups. Conclusions: Use of 40 mg of atorvastatin might decrease the levels of circulating EMPs and increase the number of circulating EPCs in patients with ICM in comparison with 10 mg of atorvastatin, and the effect might be independent of the decrease of lipids, oxLDL, and hsCRP. IntroductionStatins, serving as antiatherosclerosis drugs, can significantly decrease the rates of cardiovascular events in patients with coronary heart disease (CHD) and have been extensively administered in secondary prevention of CHD.

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“…In this regard, statins and 3-hydroxy-3-methylglutaryl-coenzyme A-reductase inhibitors may through their antiinflammatory effects on endothelial cells cause a reduction in endothelial MP release (67 ).…”

Section: Discussionmentioning

confidence: 99%

Evolving Role of Microparticles in the Pathophysiology of Endothelial Dysfunction

2013

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BACKGROUND Endothelial dysfunction is an early event in the development and progression of a wide range of cardiovascular diseases. Various human studies have identified that measures of endothelial dysfunction may offer prognostic information with respect to vascular events. Microparticles (MPs) are a heterogeneous population of small membrane fragments shed from various cell types. The endothelium is one of the primary targets of circulating MPs, and MPs isolated from blood have been considered biomarkers of vascular injury and inflammation. CONTENT This review summarizes current knowledge of the potential functional role of circulating MPs in promoting endothelial dysfunction. Cells exposed to different stimuli such as shear stress, physiological agonists, proapoptotic stimulation, or damage release MPs, which contribute to endothelial dysfunction and the development of cardiovascular diseases. Numerous studies indicate that MPs may trigger endothelial dysfunction by disrupting production of nitric oxide release from vascular endothelial cells and subsequently modifying vascular tone. Circulating MPs affect both proinflammatory and proatherosclerotic processes in endothelial cells. In addition, MPs can promote coagulation and inflammation or alter angiogenesis and apoptosis in endothelial cells. SUMMARY MPs play an important role in promoting endothelial dysfunction and may prove to be true biomarkers of disease state and progression.

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Statin decreases endothelial microparticle release from human coronary artery endothelial cells: implication for the Rho-kinase pathway

Cited by 123 publications

References 22 publications

Differences in Microparticle Release in Patients With Acute Coronary Syndrome and Stable Angina

Differences in Microparticle Release in Patients With Acute Coronary Syndrome and Stable Angina

Effect of 40 mg Versus 10 mg of Atorvastatin on Oxidized Low‐Density Lipoprotein, High‐Sensitivity C‐Reactive Protein, Circulating Endothelial‐Derived Microparticles, and Endothelial Progenitor Cells in Patients With Ischemic Cardiomyopathy

Evolving Role of Microparticles in the Pathophysiology of Endothelial Dysfunction

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