Use of endothelial progenitor cell capture stent (Genous Bio-Engineered R Stent) during primary percutaneous coronary intervention in acute myocardial infarction: Intermediate- to long-term clinical follow-up

Co, Melissa; Tay, Edgar; Lee, Chi‐Hang; Poh, Kian Keong; Low, Adrian; Lim, Jimmy; Lim, I.; Lim, Yean Teng; Tan, Huay Cheem

doi:10.1016/j.ahj.2007.08.031

Cited by 120 publications

(87 citation statements)

References 12 publications

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“…5,[11][12][13][14] The use of ex vivo expanded EPCs in animal and clinical studies has shown beneficial effects in reendothelialization and neovascularization, as well as in the prevention of hybrid graft thrombosis and rejection 11,12,15 and late stent thrombosis. 14,16 However, the mechanisms that regulate mobilization, migration, and differentiation of EPCs and their homing to sites of vascular injury are complex and involve several mediators and receptors, such as P-selectin glycoprotein ligand-1 (PSGL-1), ␣ 4 integrin, CXC chemokine receptor-2 and -4, and ␤ 1 -and ␤ 2 -integrins. [17][18][19][20] Furthermore, it has been shown that the interaction of platelets with EPCs influences their chemotaxis, adhesion, activation, and differentiation into mature ECs during vascular repair.…”

mentioning

confidence: 99%

“…1 Nevertheless, cells with progenitor and endothelial phenotypes have been generated in vitro from peripheral blood mononuclear cells (PBMCs) [2][3][4][5][6][7][8][9][10] and have shown potential therapeutic applications in vascular tissue engineering and cell-based therapy. 5,[11][12][13][14] The use of ex vivo expanded EPCs in animal and clinical studies has shown beneficial effects in reendothelialization and neovascularization, as well as in the prevention of hybrid graft thrombosis and rejection 11,12,15 and late stent thrombosis. 14,16 However, the mechanisms that regulate mobilization, migration, and differentiation of EPCs and their homing to sites of vascular injury are complex and involve several mediators and receptors, such as P-selectin glycoprotein ligand-1 (PSGL-1), ␣ 4 integrin, CXC chemokine receptor-2 and -4, and ␤ 1 -and ␤ 2 -integrins.…”

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confidence: 99%

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Endothelial Progenitor Cells Bind and Inhibit Platelet Function and Thrombus Formation

et al. 2009

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Background-Interactions of endothelial progenitor cells (EPCs) with vascular and blood cells contribute to vascular homeostasis. Although platelets promote the homing of EPCs to sites of vascular injury and their differentiation into endothelial cells, the functional consequences of such interactions on platelets remain unknown. Herein, we addressed the interactions between EPCs and platelets and their impact on platelet function and thrombus formation. Methods and Results-Cultured on fibronectin in conditioned media, human peripheral blood mononuclear cells differentiated, within 10 days of culture, into EPCs, which uptake acetylated low-density lipoprotein, bind ulex-lectin, lack monocyte/leukocyte markers (CD14, P-selectin glycoprotein ligand-1, L-selectin), express progenitor/endothelial markers (CD34, vascular endothelial growth factor receptor-2, von Willebrand factor, and vascular endothelial cadherin), and proliferate in culture. These EPCs bound activated platelets via CD62P and inhibited its translocation, glycoprotein IIb/IIIa activation, aggregation, and adhesion to collagen, mainly via prostacyclin secretion. Indeed, this was associated with upregulation of cyclooxygenase-2 and inducible nitric oxide synthase. However, the effects on platelets in vitro were reversed by cyclooxygenase and cyclooxygenase-2 inhibition but not by nitric oxide or inducible nitric oxide synthase inhibition. Moreover, in a ferric chloride-induced murine arterial thrombosis model, injection of EPCs led to their incorporation into sites of injury and impaired thrombus formation, leading to an incomplete occlusion with 50% residual flow. Conclusions-Peripheral blood mononuclear cell-derived EPCs bind platelets via CD62P and inhibit platelet activation, aggregation, adhesion to collagen, and thrombus formation, predominantly via upregulation of cyclooxygenase-2 and secretion of prostacyclin. These findings add new insights into the biology of EPCs and define their potential roles in regulating platelet function and thrombosis. Key Words: progenitor cells Ⅲ nitric oxide Ⅲ platelets Ⅲ prostaglandins Ⅲ thrombosis E ndothelial progenitor cells (EPCs) are believed to contribute to vascular biology and hemostasis. Although EPCs have been localized in cord blood, bone marrow, and peripheral blood as well as in some regenerative tissues, controversy relative to their isolation, identification, and functionality still exists. Indeed, the term EPC has been employed to describe different populations of multipotent cells that have the capability to differentiate, depending on the environmental cues, into mature endothelial cells (ECs). These cells are extremely rare in peripheral blood, but their number can be markedly increased after treatment with mobilizing cytokines or vascular trauma. 1 Nevertheless, cells with progenitor and endothelial phenotypes have been generated in vitro from peripheral blood mononuclear cells (PBMCs) 2-10 and have shown potential therapeutic applications in vascular tissue engineering and cell-based therapy. 5...

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Endothelial Progenitor Cells Bind and Inhibit Platelet Function and Thrombus Formation

et al. 2009

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“…The reported results indicate that the Genous TM stent is effective and promising [153][154][155][156] .…”

Section: Antibodymentioning

confidence: 99%

Coronary Arterial Drug-Eluting Stent: From Structure to Clinical

Wu¹,

McCarthy²

2012

Coronary Artery Diseases

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“…This is a stainless steel stent coated with murine monoclonal antihuman CD34 antibodies, which attract circulating EPCs, thereby encouraging rapid endothelialization and reducing thrombosis. The EPC capture stent appears effective in stable patients (39,40) and also in the setting of acute myocardial infarction (41).…”

Section: Stents Eluting Prohealing Agentsmentioning

confidence: 99%

Current status and future prospects of drug eluting stents for restenosis / Sadašnjost i budućnost stentova za restenozu koji otpuštaju lijekove

Patel¹,

Patel²,

Patel³

et al. 2012

Acta Pharmaceutica

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Drug-eluting stents (DESs) prevail in the treatment of carotid artery diseases in the interventional cardiology world owing to their efficacy for significant reduction of restenosis. A current successful DES requires a polymer coating for drug delivery. Clinical trials examining several pharmaceutical agents have demonstrated marked reduction in restenosis following stenting. The development of DES is one of the major revolutions in the field of interventional cardiology. The ideal drug to prevent restenosis must have an anti-proliferative and anti-migratory effect on smooth muscle cells but, on the other hand, it must also enhance re-endothelialization in order to prevent late thrombosis. Additionally, it should effectively inhibit the anti-inflammatory response after balloon induced arterial injury. Although DES have significantly reduced the angiographic restenosis rate and have improved clinical outcomes, late thrombosis and restenosis remain an important subject of ongoing research.

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Use of endothelial progenitor cell capture stent (Genous Bio-Engineered R Stent) during primary percutaneous coronary intervention in acute myocardial infarction: Intermediate- to long-term clinical follow-up

Cited by 120 publications

References 12 publications

Endothelial Progenitor Cells Bind and Inhibit Platelet Function and Thrombus Formation

Endothelial Progenitor Cells Bind and Inhibit Platelet Function and Thrombus Formation

Coronary Arterial Drug-Eluting Stent: From Structure to Clinical

Current status and future prospects of drug eluting stents for restenosis / Sadašnjost i budućnost stentova za restenozu koji otpuštaju lijekove

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