Transplantation of circulating endothelial progenitor cells restores endothelial function of denuded rabbit carotid arteries.
ABSTRACT Circulating endothelial progenitor cells (EPCs) play an important role in repair of injured vascular endothelium and neovascularization. The present study was designed to determine the effect of EPCs transplantation on the regeneration of endothelium and recovery of endothelial function in denuded carotid arteries.
Isolated mononuclear cells from rabbit peripheral blood were cultured in endothelial growth medium for 7 days, yielding EPCs. A rabbit model of common carotid artery denudation by passage of a deflated balloon catheter was used to evaluate the effects of EPCs on endothelial regeneration and vasomotor function. Immediately after denudation, autologous EPCs (10(5) cells in 200 microL saline) or 200 microL saline alone (control) were administered into the lumen of injured artery.
Four weeks after transplantation, fluorescence-labeled colonies of EPCs were found in the vessel wall. Local transplantation of EPCs as compared with saline administration accelerated endothelialization and significantly improved endothelium-dependent relaxation when assessed 4 weeks after denudation (n=4 to 5, P<0.05). Transplantation of EPCs did not affect vasomotor function of arterial smooth muscle cells. Protein array analysis of conditioned media obtained from cultured EPCs demonstrated the ability of these cells to produce and release a number of proangiogenic cytokines.
We conclude that local delivery of cultured circulating EPCs into the lumen of denuded carotid arteries accelerates endothelialization and improves endothelial function. Paracrine effects of EPCs may contribute to regenerative properties of EPCs.
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ABSTRACT: Aim. Endothelial progenitor cells repair related region by removal of damaged endothelial cells mechanically or replacing endothelial cells via migration from bone marrow to peripheric blood pool with stimulus of cytokines. Previously, it has been shown that number of these cells decrease in chronic stage of stable coronary heart disease, whereas they increase in number in acute coronary syndromes. The aim of this study is to investigate the difference in the number of endothelial progenitor cells among subgroups of acute coronary syndrome (ST elevation myocardial infarction, non-ST elevation myocardial infarction and unstable angina pectoris ) in patients hospitalized in coronary intensive care unit. Method. The study data were analysed in two steps. In the first step, it has been investigated whether there were any differences regarding endothelial progenitor cell count among three subgroups of acute coronary syndrome (n=112). In the second step, a further 13 patients who were hospitalized with a prediagnosis of unstabil angina 56 Cumhuriyet Tıp Dergisi Cumhuriyet Tıp Derg 2013; 35: 55-65 Cumhuriyet Medical Journal Cumhuriyet Med J 2013; 35: 55-65 pectoris and subsequently reported to have normal echocardiography and coronary angiography were also enrolled. The patients were divided into two groups; the patients with unstabil angina pectoris of whom no increase in cardiac enzymes detected indicating the absence of any cardiac damage and patients with normal coronary angiography findings constituted the first group (Grup A, n=41) and the patients with ST elevation myocardial infarction and non-ST elevation myocardial infarction of whom an increase in cardiac enzymes detected indicating a documented cardiac damage constituted the second group (Grup B, n=84). We investigated whether there were any differences regarding endothelial progenitor cell count between these two groups. Results. Our results indicate that the number of endothelial progenitor cells did not differ significantly among these three groups in the first step (3.87 ± 2.74, 5.46 ± 6.38 and 3.95 ± 2.94, respectively; p=0.232). The results of the statistical analysis also revealed no differences between Grup A and Grup B regarding EPC counts (3.89 ± 2.81 vs 4.80 ± 5.22;; p=0.302). Conclusion. In the light of these data, in coronary heart disease in which resistance to treatment is a topical problem despite improvements in therapeutic modalities, further clinical studies are needed about the number and the functions of these cells in the bone marrow and peripheric blood, their effects on target tissues and the factors regulating them, for theurapeutic use of these cells.
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ABSTRACT: Diabetes mellitus (DM) is a global health care issue resulting from hyperglycemia-mediated life-threatening complications. Although the use of glucose-lowering agents is routinely practiced, high dependence on medication leads to poor quality of life for DM patients. While it is still not feasible to precisely determine the critical timing when DM is truly established, perhaps the best way to reduce DM-associated mortality is to prevent it. To this end, an exploration of prognostic molecules sensitive enough to detect early physiological alteration at the initiating stage would be required. Recently discovered small noncoding molecules, microRNAs (miRs), in body fluid seem promising to be utilized as a biomarker to monitor DM initiation and progression, as it is believed that expression of circulating miRs reflects disease pathology. Current DM-related miRs were often referred to miRs differentially expressed in insulin target organs (liver, muscle, and adipose tissues) or circulating blood (peripheral blood) in diabetic patients compared to their control counterparts, although these miRs could merely be resultant nucleotides from DM-induced organ impairment instead of the indicators of onset/progression of DM. In the current review, studies showing circulating miRs associated with type 2 DM and its complications are summarized, and future scope of using miRs as biomarkers for disease prognosis/diagnosis is also emphasized.Journal of the Chinese Medical Association 12/2014; DOI:10.1016/j.jcma.2014.11.002 · 0.89 Impact Factor