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1.
It is still unclear whether the timing of intracoronary stem cell therapy affects the therapeutic response in patients with myocardial infarction.The natural course of healing the infarction and the presence of putative homing signals within the damaged myocardium appear to favor cell engraftment during the transendothelial passage in the early days after reperfusion.However,the adverse inflammatory environment,with its high oxidative stress,might be deleterious if cells are administered too early after reperfusion.Here we highlight several aspects of the timing of intracoronary stem cell therapy.Our results showed that transplantation of bone marrow mesenchymal stem cells at 2 4 weeks after myocardial infarction is more favorable for reduction of the scar area,inhibition of left ventricular remodeling,and recovery of heart function.Coronary injection of autologous bone marrow mesenchymal stem cells at 2 4 weeks after acute myocardial infarction is safe and does not increase the incidence of complications.  相似文献   

2.
摘要 目的：探讨青年初发急性心肌梗死（Acute myocardial infarction, AMI）的临床特点及其发生心功能下降的相关危险因素。方法：收集年龄＜45岁的初发AMI且行冠脉造影检查的患者86例及同期60-75岁的患者96例,对两组患者的临床资料进行对比分析,并对青年组心功能下降的危险因素进行Logistic回归分析。结果：青年组年龄中位数为40岁,男性患者及吸烟人群比例显著高于老年组（P＜0.01）,高血压及糖尿病患者的比例显著低于老年组（P＜0.001）;血尿酸水平、甘油三酯、低密度脂蛋白胆固醇均显著高于老年组,而高密度脂蛋白胆固醇及脂蛋白（a）显著低于老年组（P＜0.01）;冠脉多支病变的比例和Gensini评分低于老年组（P＜0.001）,左室射血分数＜40%的比例显著低于老年组（P＜0.01）。两组罪犯血管为前降支、回旋支及右冠脉的比例比较无明显差异（P＞0.05）。Logistic回归分析显示高尿酸和高冠脉Gensini评分是青年初发AMI患者心功能下降的危险因素（P＜0.05）。结论：青年初发AMI以男性为主,吸烟、高尿酸、血脂异常更为多见,冠脉病变严重程度相对较轻,高尿酸和冠脉Gensini评分是青年初发AMI后心功能下降的危险因素。  相似文献   

3.
Background. Myocardial blush grade (MBG) and myocardial contrast echocardiography (MCE) are both indices for myocardial perfusion in patients with ST-elevation acute myocardial infarction (STEMI). We aimed to compare MBG with MCE in the infarct-related artery segment for assessing infarct size in patients with STEMI treated with primary percutaneous coronary intervention (PCI).Methods. 43 patients underwent successful (postprocedural TIMI flow 3) primary PCI for STEMI. MBG was assessed at the end of the PCI procedure and MCE was assessed 1.7±1.8 days after PCI. Enzymatic infarct size was estimated by measurementof enzyme activities by using lactate dehydrogenase (LDH) as the referenceenzyme. Cumulative enzyme release (LDHQ48) from at least five serial measurements up to 48 hours after symptom onset was calculated. Also peak creatine kinase, CK-MB and peak LDH were measured.Results. MBG 0/1, 2 and 3 were observed in 14, 12 and 17 patients, respectively, and was compared with tertiles of MCE. We found a parallel correlation between both MBG and MCE and LDHQ48. However, there was no correlation between MCE and MBG. Patients with both normal MCE and a normal MBG had least myocardial damage and those with both impaired MCE and an impaired MBG had most myocardial damage.Conclusion. Both MBG and MCE are good predictors of infarct size in STEMI patients treated with PCI. However, these markers are not mutually related, possibly due to time-related changes in myocardial perfusion. Combining these two markers may yield a more accurate prediction of final myocardial damage. (Neth Heart J 2010;18:25-30.)  相似文献   

4.
In patients with ST-segment elevation myocardial infarction (STEMI), the time of onset of ischemia has been associated with myocardial infarction (MI) size. Myocardial blush grade (MBG) reflects myocardial response to ischemia/reperfusion injury, which may differ according to time of the day. The aim of our study was to explore the 24-hour variation in MBG and MI size in relation to outcomes in STEMI patients. A retrospective multicenter analysis of 6970 STEMI patients was performed. Time of onset of STEMI was divided into four 6-hour periods. STEMI patients have a significant 24-hour pattern in onset of symptoms, with peak onset around 09:00 hour. Ischemic time was longest and MI size, estimated by peak creatine kinase concentration, was largest in patients with STEMI onset between 00:00 and 06:00 hours. Both MBG and MI size were independently associated with mortality. Time of onset of STEMI was not independently associated with mortality when corrected for baseline and procedural factors. Interestingly, patients presenting with low MBG between 00:00 and 06:00 hours had a better prognosis compared to other groups. In conclusion, patients with symptom onset between 00:00 and 06:00 hours have longer ischemic time and consequently larger MI size. However, this does not translate into a higher mortality in this group. In addition, patients with failed reperfusion presenting in the early morning hours have better prognosis, suggesting a 24-hour pattern in myocardial protection.  相似文献   

5.
    
Detection of the optimal cell transplantation strategy for myocardial infarction (MI) has attracted a great deal of attention. Commitment of engrafted cells to angiogenesis within damaged myocardium is regarded as one of the major targets in cell‐based cardiac repair. Bone marrow–derived CD34‐positive cells, a well‐characterized population of stem cells, might represent highly functional endothelial progenitor cells and result in the formation of new blood vessels. Recently, physical microenvironment (extracellular matrix stiffness) around the engrafted cells was found to exert an essential impact on their fate. Stem cells are able to feel and respond to the tissue‐like matrix stiffness to commit to a relevant lineage. Notably, the infarct area after MI experiences a time‐dependent stiffness change from flexible to rigid. Our previous observations demonstrated myocardial stiffness‐dependent differentiation of the unselected bone marrow–derived mononuclear cells (BMMNCs) along endothelial lineage cells. Myocardial stiffness (~42 kPa) within the optimal time domain of cell engraftment (at week 1 to 2) after MI provided a more favourable physical microenvironment for cell specification and cell‐based cardiac repair. However, the difference in tissue stiffness‐dependent cell differentiation between the specific cell subsets expressing and no expressing CD34 phenotype remains uncertain. We presumed that CD34‐positive cell subsets facilitated angiogenesis and subsequently resulted in cardiac repair under induction of infarcted myocardium‐like matrix stiffness compared with CD34‐negative cells. If the hypothesis were true, it would contribute greatly to detect the optimal cell subsets for cell therapy and to establish an optimized therapy strategy for cell‐based cardiac repair.  相似文献   

6.
    
BACKGROUND: Retrovirus-mediated gene transfer is a useful technology in studying the biology of hematopoietic stem cells (HSCs) as well as in developing gene therapy products for a variety of human diseases. One of the most important factors determining the success of these studies is the number of HSCs receiving the gene of interest. METHODS: We tested various parameters for their influences on gene transfer efficiency to CD34+ cells derived from bone marrow. Based on a literature survey, three medium formulations of CD34+ cells have been compared for their effects on gene delivery efficiency and differentiation of them. We also tested whether FBS, used in the medium formulation, could be replaced with human serum or synthetic material. RESULTS: Formulation A, consisting of stem cell factor, Flt-3 ligand, thrombopoietin, and IL-3, provided optimum results in that it maintained the highest percentage of CD34+ cells during the culture as well as produced the highest gene delivery efficiency. It was found that the synthetic serum substitute containing bovine serum albumin, insulin and human transferrin could replace the fetal bovine serum present in the original formulation A without compromising gene transfer efficiency. When the transduction procedure was repeated three times, the gene could be delivered in up to 60% of the cell population. Gene delivery efficiency was comparable between CD34+ cells derived from bone marrow and mobilized peripheral blood. CONCLUSIONS: Our data could be useful in designing a procedure for stem cell gene therapy and providing a basis for further improving the conditions for gene transfer to various HSCs.  相似文献   

7.
    
We suggested that low‐level laser irradiation (LLLI) precondition prior to cell transplantation might remodel the hostile milieu of infarcted myocardium and subsequently enhance early survival and therapeutic potential of implanted bone marrow mesenchymal stem cells (BMSCs). Therefore, in this study we wanted to address: (1) whether LLLI pre‐treatment change the local cardiac micro‐environment after myocardial infarction (MI) and (2) whether the LLLI preconditions enhance early cell survival and thus improve therapeutic angiogenesis and heart function. MI was induced by left anterior descending artery ligation in female rats. A 635 nm, 5 mW diode laser was performed with energy density of 0.96 J/cm2 for 150 sec. for the purpose of myocardial precondition. Three weeks later, qualified rats were randomly received with LLLI precondition (n= 26) or without LLLI precondition (n= 27) for LLLI precondition study. Rats that received thoracotomy without coronary ligation were served as sham group (n= 24). In the cell survival study, rats were randomly divided into 4 groups: serum‐free culture media injection (n= 8), LLLI precondition and culture media injection (n= 8), 2 million male BMSCs transplantation without LLLI pre‐treatment (n= 26) and 2 million male BMSCs transplantation with LLLI precondition (n= 25) group, respectively. Vascular endothelial growth factor (VEGF), glucose‐regulated protein 78 (GRP78), superoxide dismutase (SOD) and malondialdehyde (MDA) in the infarcted myocardium were evaluated by Western blotting, real‐time PCR and colorimetry, respectively, at 1 hr, 1 day and 1 week after laser irradiation. Cell survival was assayed with quantitative real‐time PCR to identify Y chromosome gene and apoptosis was assayed with transferase‐mediated dUTP end labelling staining. Capillary density, myogenic differentiation and left ventricular function were tested by immunohistochemistry and echocardiography, respectively, at 1 week. After LLLI precondition, increased VEGF and GRP78 expression, as well as the enhanced SOD activity and inhibited MDA production, was observed. Compared with BMSC transplantation and culture media injection group, although there was no difference in the improved heart function and myogenic differentiation, LLLI precondition significantly enhanced early cell survival rate by 2‐fold, decreased the apoptotic percentage of implanted BMSCs in infarcted myocardium and thus increased the number of newly formed capillaries. Taken together, LLLI precondition could be a novel non‐invasive approach for intraoperative cell transplantation to enhance cell early survival and therapeutic potential.  相似文献   

8.
目的:观察通心络胶囊对急性心肌梗死(AMI)未接受经皮冠状动脉介入治疗(PCI)或溶栓治疗后患者的疗效。方法:对我院收治的ST段抬高未实施PCI或溶栓治疗的AMI患者,随机分为常规药物治疗作为对照组(20例)和同时加服用通心络胶囊的治疗组(20例)。于发病后一月内观察再发心绞痛、急性心血管事件、左室射血分数(LVEF)改变。结果:通心络组心功能改善较对照组明显,通心络组再发心绞痛及急性心血管事件较对照组明显减少。结论:通心络对急性心肌梗死保守治疗患者不仅减少心绞痛发作及急性心血管事件的发生而且可改善心功能。  相似文献   

9.
    
Ventricular remodeling following myocardial infarction (MI) is a major cause of heart failure, a condition prevalent in older individuals. Following MI, immune cells are mobilized to the myocardium from peripheral lymphoid organs and play an active role in orchestrating repair. While the effect of aging on mouse bone marrow (BM) has been studied, less is known about how aging affects human BM cells and their ability to regulate repair processes. In this study, we investigate the effect aging has on human BM cell responses post‐MI using a humanized chimeric mouse model. BM samples were collected from middle aged (mean age 56.4 ± 0.97) and old (mean age 72.7 ± 0.59) patients undergoing cardiac surgery, CD34+/− cells were isolated, and NOD‐scid‐IL2rγnull (NSG) mice were reconstituted. Three months following reconstitution, the animals were examined at baseline or subjected to coronary artery ligation (MI). Younger patient cells exhibited greater repopulation capacity in the BM, blood, and spleen as well as greater lymphoid cell production. Following MI, CD34+ cell age impacted donor and host cellular responses. Mice reconstituted with younger CD34+ cells exhibited greater human CD45+ recruitment to the heart compared to mice reconstituted with old cells. Increased cellular responses were primarily driven by T‐cell recruitment, and these changes corresponded with greater human IFNy levels and reduced mouse IL‐1β in the heart. Age‐dependent changes in BM function led to significantly lower survival, increased infarct expansion, impaired host cell responses, and reduced function by 4w post‐MI. In contrast, younger CD34+ cells helped to limit remodeling and preserve function post‐MI.  相似文献   

10.
    
We have chosen collagen, chitosan acetate, hyaluronic acid, and propolis as model biochemical compound solution to determine the influence of cell carrier mechanics on cell viability and functionality during and after transplantation. Suspending of bone marrow (BM), mononuclear (MN), and CD34+ cells into a biochemical compounds solution is an attractive tool to achieve to protect and ensure reproducible deliver. Hyperglycemic rats were randomly divided into 2 groups: to receive no cell treatment or approximately 1 × 105 of BM, MN, and CD34+ cells within the PBS or biochemical compound solution. These cells were infused into the hyperglycemic rats on day 10 and again on day 20. At each time point, the animals were anaesthetized with ether, and 200 μL of blood was drawn from the tail vein. Samples were collected to determine whether BM, MN, and CD34+ cell affected glucose content and insulin production. Our results exhibit the use of biochemical compound solution method to overcome the cell transplantation problem during and after injection of these cells into rats. These findings are supported by resulting in significantly greater insulin production and more decreased glucose content than cells injected in PBS only (P < 0.05). These effects displayed the following hierarchy: hyaluronic acid > chitosan acetate > collagen > propolis solution. Our results showed that these compounds demonstrated a capacity to encapsulate the BM, MN, and CD34+ cells. It is proven by decreasing glucose content and increasing insulin secretion by pancreatic cells. The uniqueness of our study is the improvement of current transplantation efficiency.  相似文献   

11.
    
Cell transplantation has become an attractive option for cardiac regenerative therapy. However, poor cell survival and extensive redistribution throughout the body can drastically affect the outcome and safety of cell therapy. Although various approaches have been attempted to support the survival and engraftment of implanted cells, we need to apply a new comprehensive strategy by melding the in vitro and in vivo approaches to recondition the cells and infarcted myocardium. Here we summarize our understanding of cell survival and migration after transplantation into the damaged heart.  相似文献   

12.
Cultured adherent bone marrow stromal cells (BMSCs) are capable of forming ectopic hematopoietic microenvironments (HMEs) in immunodeficient mice. However, the cell surface phenotype of the native bone marrow stem/progenitor cell that gives rise to BMSCs that support hematopoiesis remains poorly defined. We recently reported the derivation of human BMSC-like cells (CD133BMSCs) by magnetic cell sorting against Prominin-1 (CD133), an epitope expressed by embryonic, fetal, and adult stem cells. Here we demonstrate that CD133BMSCs are capable of forming ectopic HMEs. Cultured adherent CD133BMSCs derived from sorted CD133-positive cells lacked CD133 expression, but were uniformly positive for CD146, an epitope recently described to identify self-renewing osteoprogenitor cells that could transfer the HME. CD133BMSCs were genetically-tagged by lentivirus, expanded, and seeded into HA/TCP/fibrin constructs that were implanted subcutaneously. After 60 days, CD133BMSCs produced human osteocytes, osteoblasts, adipocytes, and reticular cells that supported murine hematopoiesis. CD133BMSCs that were not transduced with lentivirus also formed HMEs. Control constructs seeded with human dermal fibroblasts formed connective tissue, but failed to form HMEs. Our data indicate that CD133 expression identifies a native human bone marrow stem/progenitor cell that gives rise to BMSCs capable of forming the HME.  相似文献   

13.
  总被引：3，自引：0，他引：3  
Recent clinical studies have demonstrated that intracoronary infusion of autologous bone marrow cells (BMC) in conjunction with standard treatment may improve left ventricular function after an acute myocardial infarction (AMI). However, the results of these studies remain controversial, as the studies were relatively small in size and partially differed in design. We reviewed primary controlled randomized clinical studies comparing intracoronary transfer of autologous non-mobilized BMC combined with standard therapy versus standard therapy alone in patients with AMI. We identified five randomized controlled clinical trials, three of which were also placebo- and bone marrow aspiration-controlled. Non-mobilized BMC were infused into the revascularized coronary target artery 6.6 +/- 6.1 days after AMI. The mean follow- up period of 5.2 +/- 1.1 months was completed by 482 patients, 241 of which received infusion of BMC. The effect of BMC on left ventricular ejection fraction (LVEF) as a major functional parameter was evaluated. Analyzing the overall effect on the change in LVEF between baseline and follow-up value revealed a significant improvement in the BMCtreated group as compared to the control group (P = 0.04). Thus, considering the increase in LVEF during follow-up, transplantation of BMC may be a safe and beneficial procedure to support treatment of AMI. However, the functional improvement observed with this form of therapy was altogether relatively moderate and the studies were heterogeneous in design. Hence, further efforts aiming at large-scale, double-blind, randomized and placebo-controlled multi-center trials in conjunction with better definition of patients, which benefit from BMC infusion, appear to be warranted.  相似文献   

14.
    
Erythropoietin (EPO) was shown to have protective effects after myocardial infarction (MI) by neovascularization and antiapoptotic mechanisms. Beside direct receptor-dependent mechanisms, mobilization and homing of bone marrow-derived cells (BMCs) may play a pivotal role in this regard. In this study, we intended to track different subpopulations of BMCs and to assess serially myocardial perfusion changes in EPO-treated mice after MI. To allow tracking of BMCs, we used a chimeric mouse model. Therefore, mice (C57BL/6J) were sublethally irradiated, and bone marrow (BM) from green fluorescent protein transgenic mice was transplanted. Ten weeks later coronary artery ligation was performed to induce MI. EPO was injected for 3 days with a total dose of 5000 IU/kg. Subpopulations (CD31, c-kit, CXCR-4 and Sca-1) of EGFP(+) cells were studied in peripheral blood, bone marrow and hearts by flow cytometry. Myocardial perfusion was serially investigated in vivo by pinhole single-photon emission computed tomography (SPECT) at days 6 and 30 after MI. EPO-treated animals revealed an enhanced mobilization of BMCs into peripheral blood. The numbers of these cells in BM remained unchanged. Homing of all BMCs subpopulations to the ischaemic myocardium was significantly increased in EPO-treated mice. Among the investigated subpopulations, EPO predominantly affected migration of CXCR-4(+) (4.3-fold increase). Repetitively SPECT analyses revealed a reduction of perfusion defects after EPO treatment over time. Our study shows that EPO treatment after MI enhances the migration capacity of BMCs into ischaemic tissue, which may attribute to an improved perfusion and reduced size of infarction, respectively.  相似文献   

15.
    
The prognosis of patients with myocardial infarction (MI) and resultant chronic heart failure remains extremely poor despite advances in optimal medical therapy and interventional procedures. Animal experiments and clinical trials using adult stem cell therapy following MI have shown a global improvement of myocardial function. Bone marrow-derived mesenchymal stem cells (MSCs) hold promise for cardiac repair following MI, due to their multilineage, self-renewal and proliferation potential. In addition, MSCs can be easily isolated, expanded in culture, and have immunoprivileged properties to the host tissue. Experimental studies and clinical trials have revealed that MSCs not only differentiate into cardiomyocytes and vascular cells, but also secrete amounts of growth factors and cytokines which may mediate endogenous regeneration via activation of resident cardiac stem cells and other stem cells, as well as induce neovascularization, anti-inflammation, anti-apoptosis, anti-remodelling and cardiac contractility in a paracrine manner. It has also been postulated that the anti-arrhythmic and cardiac nerve sprouting potential of MSCs may contribute to their beneficial effects in cardiac repair. Most molecular and cellular mechanisms involved in the MSC-based therapy after MI are still unclear at present. This article reviews the potential repair mechanisms of MSCs in the setting of MI.  相似文献   

16.
    
Adult bone marrow‐derived very small embryonic‐like stem cells (VSEL‐SCs) exhibit a Sca‐1+/Lin–/CD45– phenotype and can differentiate into various cell types, including cardiomyocytes and endothelial cells. We have previously reported that transplantation of a small number (1 × 106) of freshly isolated, non‐expanded VSEL‐SCs into infarcted mouse hearts resulted in improved left ventricular (LV) function and anatomy. Clinical translation, however, will require large numbers of cells. Because the frequency of VSEL‐SCs in the marrow is very low, we examined whether VSEL‐SCs can be expanded in culture without loss of therapeutic efficacy. Mice underwent a 30 min. coronary occlusion followed by reperfusion and, 48 hrs later, received an intramyocardial injection of vehicle (group I, n= 11), 1 × 105 enhanced green fluorescent protein (EGFP)‐labelled expanded untreated VSEL‐SCs (group II, n= 7), or 1 × 105 EGFP‐labelled expanded VSEL‐SCs pre‐incubated in a cardiogenic medium (group III, n= 8). At 35 days after myocardial infarction (MI), mice treated with pre‐incubated VSEL‐SCs exhibited better global and regional LV systolic function and less LV hypertrophy compared with vehicle‐treated controls. In contrast, transplantation of expanded but untreated VSEL‐SCs did not produce appreciable reparative benefits. Scattered EGFP+ cells expressing α‐sarcomeric actin, platelet endothelial cell adhesion molecule (PECAM)‐1, or von Willebrand factor were present in VSEL‐SC‐treated mice, but their numbers were very small. No tumour formation was observed. We conclude that VSEL‐SCs expanded in culture retain the ability to alleviate LV dysfunction and remodelling after a reperfused MI provided that they are exposed to a combination of cardiomyogenic growth factors and cytokines prior to transplantation. Counter intuitively, the mechanism whereby such pre‐incubation confers therapeutic efficacy does not involve differentiation into new cardiac cells. These results support the potential therapeutic utility of VSEL‐SCs for cardiac repair.  相似文献   

17.
Thrombolytic agents are being employed clinically in increasing numbers of patients in the attempt to eliminate occlusive coronary thrombi in patients with evolving myocardial infarction. When administered by the intracoronary route, streptokinase lyses is successful in coronary thrombi in more than two-thirds of patients, but when administered intravenously is successful in only one-third. Since streptokinase is a nonselective plasminogen activator, it induces fibrinogenolysis when administered selectively or systematically with an attendant marked reduction in plasma fibrinogen levels and significant bleeding complications. In contrast, the action of tissue plasminogen activator (t-Pa) is relatively selective for fibrinolysis (as opposed to fibrinogenolysis). It induces coronary thrombolysis in at least 60% of patients when administered either into a coronary ostium or a peripheral vein without producing substantial reductions in circulating fibrinogen. Bleeding complications are modest and usually related to high administered doses and concomitant heparinization, and occur primarily at sites of vascular access. Thus, t-Pa appears to be a promising agent for thrombolytic treatment of patients with evolving acute myocardial infarction.  相似文献   

18.
    
Reperfusion injury following myocardial infarction (MI) increases infarct size (IS) and deteriorates cardiac function. Cardioprotective strategies in large animal MI models often failed in clinical trials, suggesting translational failure. Experimentally, MI is induced artificially and the effect of the experimental procedures may influence outcome and thus clinical applicability. The aim of this study was to investigate if invasive surgery, as in the common open chest MI model affects IS and cardiac function. Twenty female landrace pigs were subjected to MI by transluminal balloon occlusion. In 10 of 20 pigs, balloon occlusion was preceded by invasive surgery (medial sternotomy). After 72 hrs, pigs were subjected to echocardiography and Evans blue/triphenyl tetrazoliumchloride double staining to determine IS and area at risk. Quantification of IS showed a significant IS reduction in the open chest group compared to the closed chest group (IS versus area at risk: 50.9 ± 5.4% versus 69.9 ± 3.4%, P = 0.007). End systolic LV volume and LV ejection fraction measured by echocardiography at follow‐up differed significantly between both groups (51 ± 5 ml versus 65 ± 3 ml, P = 0.033; 47.5 ± 2.6% versus 38.8 ± 1.2%, P = 0.005). The inflammatory response in the damaged myocardium did not differ between groups. This study indicates that invasive surgery reduces IS and preserves cardiac function in a porcine MI model. Future studies need to elucidate the effect of infarct induction technique on the efficacy of pharmacological therapies in large animal cardioprotection studies.  相似文献   

19.
We used human angiopoietin-1 (hAng1)-modified mesenchymal stem cells (MSCs) to treat acute myocardial infarction (AMI) in rats. The hAng1 gene was transfected into cultured rat MSCs using an adenoviral vector. Five million hAng-transfected MSCs (MSC(Ang1)) or green fluorescent protein transfected MSCs (MSC(GFP)) or PBS only (PBS group) were injected intramyocardially into the inbred Lewis rat hearts immediately after myocardial infarction. MSC(Ang1) survived in the infarcted myocardium, and expressed hAng1 at both mRNA and protein levels. The vascular density was higher in the MSC(Ang1) and MSC(GFP) groups than in the PBS group. The measurements of infarcted ventricular wall thickness, infarction area, and left ventricular diameter indicated that heart remodeling was inhibited and heart function was improved in both the MSC(Ang1) and MSC(GFP) groups. However, in contrast to the MSC(GFP) group, the MSC(Ang1) group showed enhanced angiogenesis and arteriogenesis (by 11-35%), infarction area was reduced by 30% and the left ventricular wall was 46% thicker (P<0.05). The results indicated that hAng1-modified MSCs improved heart function, followed by angiogenic effects in salvaging ischemic myocardium and reduced cardiac remodeling.  相似文献   

20.
    
Cell-based therapy is considered a novel and potentially new strategy in regenerative medicine. But the efficacy of cell-based therapy has been limited by the poor survival of the transplanted cells in an ischaemic environment. The goal of the present study is to present a possibility to increase survival of the transplanted cardiomyocytes, by increasing the vascularization of the infarcted area. First, we injected endothelial progenitor cells (EPCs) to augment the vascular density in infarcted areas and to improve the benefit of a subsequent Tx of foetal cardiomyocytes. Serial echocardiography indeed showed significant improvement of the left ventricular function after application of EPC and a significant additive improvement after Tx of foetal cardiomyocytes. In contrast, repetitive EPC transplantation as a control group did not show an additional improvement after the second transplantation. Histologically, cells could be readily detected after Tx by BrdU-staining for EPC and by carboxy-fluorescein diacetate succinimidyl ester (CFSE)-staining for foetal cardiomyocytes. Staining for CD31 revealed a significant increase in vessel density in the infarction area compared with medium controls, possibly contributing to the benefit of transplanted foetal cardiomyocytes. Notably, a significant increase in the number of apoptotic cells was observed in cell-transplanted hearts accompanied by an increase in proliferation, collagen content and neutrophil infiltration, suggesting an active remodelling concomitant with sustained inflammatory processes. In conclusion, repetitive Tx of different cell types after myocardial infarction in rat hearts significantly improved left ventricular function and could represent a feasible option to enhance the benefit of cell therapy.  相似文献   

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