Endothelial progenitor cells in cardiovascular disorders

The important role of the vascular endothelium in cardiovascular health is increasingly recognized. However, mature endothelial cells possess limited regenerative capacity. There is therefore much interest in circulating endothelial progenitor cells (EPCs) among the scientific community, especially into their purported role in maintenance of endothelial integrity and function, as well as postnatal neovascularization. It has been suggested that these cells might not only be responsible for the continuous recovery of the endothelium after injury/damage, but also might take part in angiogenesis, giving the hope of new treatment opportunities. Indeed, there is accumulating evidence showing reduced availability and impaired EPC function in the presence of both cardiovascular disease and associated comorbid risk factors. Thus, many studies into the potential for use of EPCs in the clinical setting are being undertaken. The goal of this review article is to provide an overview of data relevant to the clinical role of EPCs and perspectives for treatment of cardiovascular disorders.     

Endothelial progenitor cells for cardiovascular regeneration

Endothelial progenitor cells (EPCs) are peripheral blood mononuclear cells that can differentiate into mature endothelial cells. Adult EPCs were first discovered in human peripheral blood in 1997. Since then, the potency of EPCs for cardiovascular regeneration has been demonstrated in several preclinical studies; and investigators are beginning to evaluate the therapeutic utility of EPCs in early-phase clinical trials. This review summarizes the progression of basic, preclinical, and clinical research into the potential use of EPC therapy for cardiovascular regeneration.     

Endothelial progenitor cells and cardiovascular homeostasis: clinical implications

Emerging evidences indicate that endothelial progenitor cells (EPCs) actively contribute in regulating cardiovascular homeostasis, and interest is growing for possible future diagnostic and therapeutic applications in the cardiovascular arena. In the present clinically-oriented review, special attention was given to the clinical implications of the potential of EPCs to test and strengthen the capacity of the organism to challenge atherosclerosis, vascular remodelling and ischemia. Accumulating data suggest that the vasculo-protective functions of EPCs may be used as cellular biomarkers for endothelial damage, or may be pharmacologically modulated to enhance the body's defence to atherosclerosis. Furthermore, biomedical engineering and cell transplantation open new scenarios to reverse vascular and graft remodelling and achieve therapeutic angiogenesis in limb and heart ischemia. However, a number of unsolved issues remain to be exploited, such as the identification of the true identity of EPCs and a better characterization of their role in vascular homeostasis under normal and pathologic conditions.     

Endothelial progenitor cells,cardiovascular risk factors and lifestyle modifications

Endothelial progenitor cells (EPCs) contribute substantially to preservation of a structurally and functionally intact endothelium. EPCs home in to the sites of endothelial injury and ischemia, where they proliferate, differentiate and integrate into the endothelial layer or exert a paracrine function by producing vascular growth factors. This review will focus on successful lifestyle interventions that aim to maintain vascular health through beneficial actions on cell populations with vasculogenic potential. The results of the studies proving the role of healthy lifestyle are particularly emphasized.     

Endothelial progenitor cells: a new target for the prevention of cardiovascular diseases.

Endothelial progenitor cells (EPCs) are circulating precursor cells that have been implicated recently in vascular and cardiac regeneration. There is an ongoing discussion on the immunocytological definition of EPCs, based on various surface markers, and currently different cell types are included in the term 'EPC'. This review summarizes the mechanisms that influence function, survival, mobilization and differentiation of EPCs. Furthermore, there are several reports on the clinical use of EPCs for the treatment of cardiovascular diseases. We have focused specifically on the influence of physical activity on EPC function.     

Endothelial progenitor cells: a promising therapeutic alternative for cardiovascular disease

The integrity and functional activity of the endothelial monolayer play a critical role in preventing atherosclerotic disease progression. Endothelial cell (EC) damage by atherosclerosis risk factors can result in EC apoptosis with loss of the integrity of the endothelium. Thus, approaches to repair the injured vessels with the goal of regenerating ECs have been tested in preclinical experimental models and in clinical studies. Indeed, endothelial progenitor cells (EPCs) originating from the bone marrow have been shown to incorporate into sites of neovascularization and home to sites of endothelial denudation. These cells may provide an endogenous repair mechanism to counteract ongoing risk factor-induced endothelial injury and to replace dysfunctional endothelium. Risk factors for coronary artery disease, such as age, smoking, hypertension, hyperlipidemia, and diabetes, however, reduce the number and functional activity of circulating EPCs, potentially restricting the therapeutic prospective of progenitor cells and limiting the regenerative capacity. Furthermore, the impairment of EPCs by risk factors may contribute to atherogenesis and atherosclerotic disease progression. The article reviews the role of EPCs in atherogenesis and in predicting cardiovascular outcomes, and highlights the potential challenges in developing therapeutic strategies aiming to interfere with the balance of injury and repair mechanisms.     

Endothelial progenitor cells participate in nicotine-mediated angiogenesis.

OBJECTIVES: We aimed to determine the role of endothelial progenitor cells (EPCs) in cholinergic angiogenesis. BACKGROUND: Recently, we provided evidence for a new angiogenic pathway mediated by endothelial nicotinic acetylcholine receptors (nAChR). Increasing evidence suggests that circulating EPCs also contribute to postnatal neovascularization by homing to sites of neovascularization, a process termed postnatal vasculogenesis. Therefore, we investigated whether nAChR activation increases mobilization and/or recruitment of EPCs to a site of angiogenesis. METHODS: To identify EPCs from reservoirs both inside and outside of the bone marrow and to avoid the adverse effects of total body irradiation, we employed a murine parabiosis model with tie-2-LacZ FvB/N mice connected to wild-type FvB/N mice and induced unilateral hind limb ischemia in the wild-type animal. RESULTS: Administration of nicotine increased capillary density in the ischemic hind limb, and increased soluble Kit ligand plasma levels. The effect of systemic administration was greater than that of local delivery of nicotine (45% vs. 76% increase in capillary density by comparison to vehicle control, intramuscular vs. oral administration of nicotine; p < 0.05). Ischemia-induced incorporation of EPC in the control group was rare, but was increased 5-fold by systemic administration of nicotine. Exposure to nicotine in vitro increased EPC count and EPC transmigration. Finally, systemic administration of nicotine increased EPC number in the bone marrow and spleen during hind limb ischemia. CONCLUSIONS: Nicotine treatment increased the number of EPCs in the bone marrow and spleen, and increased their incorporation into the vasculature of ischemic tissue. Administration of nicotine increased markers of EPC mobilization. This study indicates that the known angiogenic effect of nicotine may be mediated in part by mobilization of precursor cells.     

Endothelial progenitor cells and erectile dysfunction.

Baumhäkel and coworkers have recently examined the levelsof circulating CD34⁺KDR⁺ and CD133⁺ cells in patients with coronaryartery disease (CAD), which were evaluated for the presenceof erectile dysfunction (ED). They show that CD133⁺,     

Endothelial progenitor cells in infantile hemangioma

Infantile hemangioma is an endothelial tumor that grows rapidly after birth but slowly regresses during early childhood. Initial proliferation of hemangioma is characterized by clonal expansion of endothelial cells (ECs) and neovascularization. Here, we demonstrated mRNA encoding CD133-2, an important marker for endothelial progenitor cells (EPCs), predominantly in proliferating but not involuting or involuted hemangioma. Progenitor cells coexpressing CD133 and CD34 were detected by flow cytometry in 11 of 12 proliferating hemangioma specimens from children 3 to 24 months of age. Furthermore, in 4 proliferating hemangiomas, we showed that 0.14% to 1.6% of CD45(-) nucleated cells were EPCs that coexpressed CD133 and the EC marker KDR. This finding is consistent with the presence of KDR(+) immature ECs in proliferating hemangioma. Our results suggest that EPCs contribute to the early growth of hemangioma. To our knowledge, this is the first study to show direct evidence of EPCs in a human vascular tumor.     

内皮祖田胞与血管新生

某些缺血性疾病,如冠心病、脑血管病变等在发生发展的过程中有血管的闭塞和退化,因此,当今心血管病学中一个重要的进展就是兴起了促进新生血管生成的治疗.     

Endothelial progenitor cells functional characterization

Increasing evidence suggests that circulating progenitor cells contribute to postnatal neovascularization. These cells home to sites of ischemia, adopt an endothelial phenotype, and contribute to new blood vessel formation. Hence, the identity of the circulating cells that contribute to neovascularization is not entirely clear. Bone-marrow-derived hematopoietic progenitor cells can give rise to endothelial cells and contribute to endothelial recovery and new capillary formation after ischemia. However, nonhematopoietic stem cells within the bone marrow and adipose-tissue-derived cells, as well as cardiac and neural progenitor cells, also differentiate to endothelial cells. Progenitor cells from the different sources may be useful to augment therapeutic vascularization. The present review article summarizes the different subtypes of (endothelial) progenitor cells that can give rise to endothelial cells, enhance neovascularization, and may be suitable for therapeutic neovascularization.     

内皮祖细胞在急性肺损伤中的应用

急性肺损伤(acute lung injury,ALI)是临床常见危重症,目前缺乏有效的治疗手段,病死率高达40%[1].内皮细胞的损伤和活化在ALI发病机制中占有极其重要的地位[2].     

Endothelial progenitor cells in patients with essential hypertension

OBJECTIVE(S): The eventual role of blood pressure on the endothelial progenitor cell (EPC) has rarely been evaluated and data collected so far relate to patients with co-existing coronary heart disease. METHODS: We have studied the number and functional activity of EPC as well as the number of EPC endothelial colony-forming units (CFU) in a carefully selected group of 36 patients with essential hypertension and 24 normotensive control subjects. RESULTS: In patients with essential hypertension, the EPC number was not statistically different from that found in control subjects (mean +/- SD, essential hypertension 58 +/- 29, controls 53 +/- 20; EPC/high power field). CFU per well were not statistically different in patients with essential hypertension compared with normotensive controls (mean +/- SD, patients with essential hypertension 2.4 +/- 2.6, normotensive controls 3 +/- 3.3 CFU/well). In essential hypertension patients, the EPC number was inversely correlated with both total (R=0.635, P < 0.0001) and low-density lipoprotein (LDL)-cholesterol (R=0.486, P < 0.05). Neither the EPC number nor the EPC CFU were correlated with age, systolic blood pressure, diastolic blood pressure, body mass index, lipoprotein(a), high-sensitivity C-reactive protein or homocysteine. CONCLUSIONS: The present study shows that essential hypertension is not characterized by the altered number or functional activity of EPC. Plasma total and LDL-cholesterol are independent predictors of reduced numbers of circulating EPC in essential hypertension patients. The absence of any correlation between the characteristics of EPC and several markers predictive of cardiovascular damage merits further investigation.