The Role of Endothelial Progenitor Cells in the Cardiovascular Disease Pathogenesis

Nicoleta Alexandru¹, Elisabeta Badila² and Adriana Georgescu¹*

¹Department of Pathophysiology and Pharmacology, Institute of Cellular Biology and Pathology, ‘Nicolae Simionescu’ of Romanian Academy, Romania

²Emergency Hospital Bucharest, Romania

*Corresponding author: Adriana Georgescu, Department of Pathophysiology and Pharmacology, Institute of Cellular Biology and Pathology ‘Nicolae Simionescu’ of Romanian Academy 8, BP Hasdeu Street, PO Box 35-14, 050568-Bucharest, Romania

Received: Aug 23, 2014; Accepted: Aug 23, 2014; Published: Aug 25, 2014

Editorial

The development of atherosclerosis and cardiovascular disease is the result of multiple intermediate processes where endothelial dysfunction and vascular inflammation play key contributing roles. Atherosclerosis is one of the most important and common cause of death and disability in the world and remains an occult but important precursor of significant cardiovascular events. Atherosclerosis as a chronic inflammatory disease of the arterial wall is closely related to subendothelial lipoprotein retention, endothelial activation and migration of immune cells to inflamed intima which result in formation of fatty streaks and subsequent atheromas [1,2].

Endothelial Progenitor Cells (EPCs) have attracted major interest as biomarkers and potential regulators for atherosclerotic vascular disease, but their involvement in the mechanisms of inflammatory processes and vascular repair remain controversial. EPCs are present in peripheral blood and can develop a functional endothelial phenotype. The number and function of circulating EPCs are altered in atherosclerosis, diabetes, chronic venous insufficiency and EPCs have been shown to promote postnatal angiogenesis and vasculogenesis [3-7]. In contrast, elevated EPC levels were seen in patients that suffered an acute myocardial infarction [8] and patients that underwent a percutaneous coronary intervention [9]. Also, in patients with coronary artery disease some studies report that the EPC number is increased [10,11]. Besides, patients with unstable angina and no evidence of cardiac necrosis exhibited increased circulating EPCs [3]. Systemic inflammation, in addition to recognized growth factors, could play a role in the peripheral mobilisation of EPCs in these patients. Likewise, it can be speculated that this may represent a protective, compensatory response.

In this context, EPC research has important clinical implications but is often impeded by methodological issues and a lack of consensus on phenotypic identification of these cells.

The number of circulating EPCs can be measured using fluorescence-activated cell-sorting analysis and standard gating techniques to detect surface marker expression [12]. Asahara et al. [13] was the first to isolate EPCs in human peripheral blood, using anti-CD34 monoclonal antibodies. Now EPCs are defined as either early and late EPCs based on their biological properties and their time of appearance in vitro culture. With the use of CD133, an antigen specifically identifying primitive stem cells, a novel means to precisely delineate mature from immature EPCs was possible [14]. Other markers used include vWF, VE-cadherin, Vascular Endothelial Growth Factor Receptor-2 (VEGFR-KDR) and binding by lectins and Acetylated Low-Density Lipoproteins (Ac-LDL) [14-16].

The EPC function can, in part, be measured by assessing their colony forming capacity in vitro [17]. Modalities to increase the number or improve the function of EPCs may be promising in the treatment of cardiovascular disease. Among these are physical exercise, administration of erythropoietin and treatment with statins [18] and irbesartan [6,19], which enhance both the number and functionality of EPCs. In addition, systemic transfusion of EPCs improves the endothelial and platelet function and reduces the atherosclerosis in the animal models [20,21]. EPCs have the ability to reduce platelet activation and to modulate their pro-inflammatory and antithrombogenic properties in hypertension associated with hypercholesterolemia. These findings revealed a new biological role of circulating EPCs in platelet function regulation, and contributed to a better understanding of their crosstalk, and the mechanisms of atherosclerosis [21].

However, much work remains to be done to clarify the role of EPCs in cardiovascular disease. Presently, there is a huge interest in the EPC assessment as advanced markers for cardiovascular disease pathogenesis evaluation and drug therapy monitoring.

The Role of Endothelial Progenitor Cells in the Cardiovascular Disease Pathogenesis

Editorial

References