Association of multiple blood metals and systemic atherosclerosis: A cross-sectional study in the CAD population.

BACKGROUND: Coronary atherosclerotic disease (CAD) is often accompanied by peripheral atherosclerosis, resulting in a higher risk of ischemia and cardiovascular death. Exposure to metals is associated with atherosclerotic plaques at specific sites. However, less is known about the effects of mixed metals on systemic atherosclerotic burden in CAD patients. OBJECTIVES: To investigate the association of metal mixtures with systemic atherosclerotic burden in a CAD population. METHODS: A cross-sectional study including 1562 CAD patients from Southwest China was conducted. The levels of 10 blood metals were measured via inductively coupled plasma spectrometry. More than one vessel with a stenosis ≥50% vessel diameter was defined as CAD. Carotid and lower limb atherosclerosis was assessed by using ultrasound, and coronary atherosclerosis was quantified via arterial angiography. Systemic atherosclerosis was scored according to the presence or absence of lesions at the three sites and the total number of lesions. To investigate the combined impacts and interaction effects of metals, Bayesian kernel machine regression was used. Weighted quantile regression was used to identify the contributions of the metals. RESULTS: Significant overall associations of mixed metals with systemic atherosclerotic burden were found. These positive overall associations were mainly driven by Cd, Cu and Pb in systemic atherosclerosis. The main contributing factors were As and Cu for coronary atherosclerosis as well as Cd, Cu and Pb for carotid and lower limb atherosclerosis. Cd and Pb or Cr can interact, and Pb interacts with age, sex and alcohol. CONCLUSIONS: In CAD patients, exposure to combinations of metals was highly positively associated with systemic atherosclerotic burden. These significant trends were more pronounced in the peripheral arteries and carotid arteries. Controlling environmental metal exposure can contribute to reducing systemic atherosclerosis in CAD patients.

The effect of fine particulate matter on atherosclerosis and its mechanism / 预防医学

@#Fine particulate matter (PM2.5) not only directly damages lung tissue, but also can be absorbed into blood through alveolar capillaries, which is toxic to the cardiovascular system. PM2.5 can affect lipid metabolism, endothelial function, coagulation and thrombosis through oxidative stress, inflammatory reaction, autonomic nervous dysfunction and immune regulation abnormality, so that it promote arteriosclerosis, plaque instability, and increase the morbidity and mortality of cardiovascular disease. We reviewed the effects and mechanisms of PM2.5 on arteriosclerosis, in order to provide the evidence for the studies into prevention of cardiovascular diseases caused by air pollution.

Transplantation of EPCs overexpressing PDGFR-ß promotes vascular repair in the early phase after vascular injury.

BACKGROUND: Endothelial progenitor cells (EPCs) play important roles in the regeneration of the vascular endothelial cells (ECs). Platelet-derived growth factor receptor (PDGFR)-ß is known to contribute to proliferation, migration, and angiogenesis of EPCs, this study aims to investigate effects of transplantation of EPCs overexpressing PDGFR-ß on vascular regeneration. METHODS: We transplanted genetically modified EPCs overexpressing PDGFR-ß into a mouse model with carotid artery injury. After 3 days of EPCs transplantation, the enhanced green fluorescent protein (EGFP)-expressing cells were found at the injury site and the lining of the lumen by laser scanning confocal microscope (LSCM). At 4, 7, and 14 days of the carotid artery injury, reendothelialization was evaluated by Evans Blue staining. Neointima formation was evaluated at day 14 with hematoxylin and eosin (HE) staining by calculating the neointimal area, medial area, and neointimal/media (NI/M) ratio. Intimal cell apoptosis was evaluated using TUNEL assay. Then we tested whether PDGF-BB-induced VSMC migration and PDGF-BB's function in reducing VSMC apoptosis can be attenuated by EPCs overexpressing PDGFR-ß in a transwell co-culture system. RESULTS: Our results showed that EPCs overexpressing PDGFR-ß accelerates reendothelialization and mitigates neointimal formation at 14 days after injury. Moreover, we found that there is great possibility that EPCs overexpressing PDGFR-ß enhanc VSMC apoptosis and suppress VSMC migration by competitive consumption of PDGF-BB in the early phase after carotid artery injury in mice. CONCLUSIONS: We report the first in vivo and in vitro evidence that transplantation of genetically modified EPC can have a combined effect of both amplifying the reendothelialization capacity of EPCs and inhibiting neointima formation so as to facilitate better inhibition of adverse remodeling after vascular injury.

Transplantation of cryopreserved human umbilical cord blood-derived endothelial progenitor cells induces recovery of carotid artery injury in nude rats.

INTRODUCTION: Transplantation of endothelial progenitor cells (EPCs) restores endothelial function in patients with endothelial dysfunction and initial denudation. The goal of the present study was to determine the effect of cryopreserved human umbilical cord blood (UCB)-derived EPC infusion on the repair of carotid artery injury in nude rats. METHODS: Mononuclear cells (MNCs) from human cryopreserved UCB and peripheral blood (PB) of patients with cardiovascular diseases and healthy volunteers were cultured in a conditioned medium. The in vitro migration, proliferation, adhesion, and survival capacities, as well as paracrine cytokine release of EPCs were investigated. EPC homing, induced reendothelialization, and the effect on neointima formation were also assessed in vivo. RESULTS: Patient-derived PB EPCs (PPB-EPCs) displayed decreased migration, proliferation, adhesion, and survival capabilities as compared to PB-EPCs from healthy volunteers (HPB-EPCs) and cryopreserved UCB-EPCs. However, there was no difference in the release of vascular endothelial growth factor (VEGF) and stromal cell derived factor 1 (SDF-1) between the three groups. Two weeks after transplantation, more labeled UCB-EPCs and HPB-EPCs than PPB-EPCs were found by cell tracking in the injury zone. Administration of PPB-EPCs, HPB-EPCs, and UCB-EPCs enhanced reendothelialization and inhibited neointima formation compared to the saline control. However, UCB-EPC and HPB-EPC infusion showed a greater improvement than PPB-EPCs. CONCLUSIONS: Cryopreserved UCB-MNCs derived EPCs and HPB-EPCs show better responses to cytokines and vascular injury than PPB-EPCs. Thus, cryopreservation and delivery of cryopreserved autogenous UCB-EPCs or HPB-EPCs may be a promising vasculoprotective approach for patients with multiple cardiovascular risk factors.

Safety and efficacy of biodegradable drug-eluting vs. bare metal stents: a meta-analysis from randomized trials.

BACKGROUND: Biodegradable polymeric coatings have been proposed as a promising strategy to enhance biocompatibility and improve the delayed healing in the vessel. However, the efficacy and safety of biodegradable polymer drug-eluting stents (BP-DES) vs. bare metal stents (BMS) are unknown. The aim of this study was to perform a meta-analysis of randomized controlled trials (RCTs) comparing the outcomes of BP-DES vs. BMS. METHODS AND RESULTS: PubMed, Embase, and Cochrane Central Register of Controlled Trials (CENTRAL) were searched for randomized clinical trials, until December 2013, that compared any of approved BP-DES and BMS. Efficacy endpoints were target-vessel revascularization (TVR), target-lesion revascularization (TLR) and in-stent late loss (ISLL). Safety endpoints were death, myocardial infarction (MI), definite stent thrombosis (DST). The meta-analysis included 7 RCTs with 2,409 patients. As compared with BMS, there was a significantly reduced TVR (OR [95% CI] = 0.37 [0.28-0.50]), ISLL (OR [95% CI] = -0.41 [-0.48-0.34]) and TLR (OR [95% CI] = 0.38 [0.27-0.52]) in BP-DES patients. However, there were no difference for safety outcomes between BP-DES and BMS. CONCLUSIONS: BP-DES is more effective in reducing ISLL, TVR and TLR, as safe as standard BMS with regard to death, ST and MI. Further large RCTs with long-term follow-up are warranted to better define the relative merits of BP-DES.

[Platelet derived growth factor receptor ß over-expression in endothelial progenitor cells promote reendothelialization after vascular injury].

OBJECTIVE: To observe the effect of platelet derived growth factor receptor ß (PDGFR-ß) transfected endothelial progenitor cells (EPCs) on vascular regeneration. METHODS: Spleen-derived mononuclear cells (MNCs) were isolated using density gradient centrifugation and induced with special culture medium. EPCs transfection was performed with Lipofectamine(TM) 2000 reagent according to the instruction manual. Carotid artery injury was induced in splenectomized mice. EPCs were injected by tail vein immediately and at 24 h after endothelial injury of the carotid artery. Evans blue staining was performed to evaluate reendothelialization at 7 days after endothelial injury of the carotid artery. RESULTS: Most adherent cells were LDL and UEA-I double positive. Laser scanning confocal microscopy showed that transfection efficiency was about 50%-60%. The reendothelialized area in the PDGFR-ß-EPCs group was significantly larger than that in EGFP-EPCs group. CONCLUSION: Transplantation of PDGFR-ß over-expressed EPCs can promote reendothelialization in the early phase after carotid artery injury.

Over-expression of PDGFR-ß promotes PDGF-induced proliferation, migration, and angiogenesis of EPCs through PI3K/Akt signaling pathway.

The proliferation, migration, and angiogenesis of endothelial progenitor cells (EPCs) play critical roles in postnatal neovascularization and re-endothelialization following vascular injury. Here we evaluated whether the over-expression of platelet-derived growth factor receptor-ß (PDGFR-ß) can enhance the PDGF-BB-stimulated biological functions of EPCs through the PDGFR-ß/phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. We first confirmed the expression of endogenous PDGFR-ß and its plasma membrane localization in spleen-derived EPCs. We then demonstrated that the PDGFR-ß over-expression in EPCs enhanced the PDGF-BB-induced proliferation, migration, and angiogenesis of EPCs. Using AG1295 (a PDGFR kinase inhibitor), LY294002 (a PI3K inhibitor), and sc-221226 (an Akt inhibitor), we further showed that the PI3K/Akt signaling pathway participates in the PDGF-BB-induced proliferation, migration, and angiogenesis of EPCs. In addition, the PI3K/Akt signaling pathway is required for PDGFR-ß over-expression to enhance these PDGF-BB-induced phenotypes.

Resveratrol protects against hyperglycemia-induced oxidative damage to mitochondria by activating SIRT1 in rat mesangial cells.

Oxidative stress and mitochondrial dysfunction are involved in the pathogenesis of diabetic nephropathy (DN). Resveratrol has potent protective effects on diabetes and diabetic complications including diabetic nephropathy. We aimed to investigate the protective effects of resveratrol on mitochondria and the underlying mechanisms by using an in vitro model of hyperglycemia. We exposed primary cultured rat mesangial cells to high glucose (30mM) for 48h. We found that pretreatment with resveratrol (10µM) 6h prior to high glucose treatment significantly reduced hyperglycemia-induced increase in reactive oxygen species (ROS) production and mitochondrial superoxide generation, as well as stimulated MnSOD activity. In addition, resveratrol pretreatment significantly reversed the decrease of mitochondrial complex III activity in glucose-treated mesangial cells, which is considered to be the major source of mitochondrial oxidative stress in glucose-treated cells. Furthermore, resveratrol pretreatment efficiently restored the hyperpolarization of ∆Ψm, increased ATP production and preserved the mtDNA content. All of these protective effects of resveratrol were successfully blocked by siRNA targeting SIRT1 and EX-527, a specific inhibitor of SIRT1 activity. Our results indicated that resveratrol efficiently reduced oxidative stress and maintained mitochondrial function related with activating SIRT1 in glucose-treated mesangial cells. It suggested that resveratrol is pharmacologically promising for treating diabetic nephropathy.

Transplantation of endothelial progenitor cells overexpressing endothelial nitric oxide synthase enhances inhibition of neointimal hyperplasia and restores endothelium-dependent vasodilatation.

Endothelial progenitor cells (EPCs) play an important role in vascular repair. We hypothesized that overexpression of endothelial nitric oxide synthase (eNOS) in EPCs enhances inhibition of neointimal hyperplasia and restores endothelium-dependent vasodilatation in injured vessels. Bone marrow-derived EPCs were cultured and expanded in endothelial basal medium. EPCs were transduced with pseudotyped retroviral vectors expressing human eNOS (eNOS-EPCs) or green fluorescent protein (GFP-EPCs). Three days after gene transfer, EPC proliferation and NO production were assayed. Rats received 2×10(6) fluorescently labeled EPCs with expressing eNOS, GFP or saline by tail vein injection directly after balloon injury and again 24h later. Two weeks after transplantation, cell tracking showed that transfused EPCs could return to the injury site. Both eNOS-EPCs transplantation (p<0.05) and GFP-EPCs transplantation (p<0.05) could inhibit neointimal hyperplasia compared with saline injection. The antiproliferative effect of EPCs was further enhanced by overexpression of eNOS (p<0.05, eNOS-EPCs vs. GFP-EPCs). Furthermore, eNOS-EPCs transplantation increased significantly endothelium-dependent vasodilatation compared with GFP-EPCs transplantation. We conclude that transplantation of EPCs overexpressing eNOS could repair the injured vessel by inhibiting neointimal hyperplasia and restoring vascular function. Therefore, gene modified EPCs facilitates the strategy of cell transplantation for vascular dysfunction and restenosis after angioplasty.

Carotid artery wire injury mouse model with a nonmicrosurgical procedure.

A mouse model of endothelial denudation in the common carotid artery is usually established with a flexible wire under a dissecting microscope. In this article, we introduce a modified procedure to establish a carotid arterial injury mouse model in which no dissecting microscope is used. In the nonmicrosurgical procedure, carotid clamps, which were used to block the blood flow of the common carotid artery and the internal carotid artery, were substituted with silk slipknots. Curved flexible wire, which was used to introduce carotid artery injury, was tailored so that it could be inserted into the external carotid artery easily. A tailored hook was used to place silk around the external carotid artery and the internal carotid artery. The data show that the nonmicrosurgical procedure could achieve an effect in endothelial denudation and neointima formation similar to that of the microsurgical procedure. The operating achievement ratio and survival rates at 1 day and 4 weeks are also similar between the two groups. The operating time was reduced significantly in the nonmicrosurgical group compared to the microsurgical group. The present study suggests that establishing a carotid arterial injury mouse model with a nonmicrosurgical procedure is simple, effective, and time-saving.

The spleen recruits endothelial progenitor cell via SDF-1/CXCR4 axis in mice.

Endothelial progenitor cell (EPC) therapy represents a novel strategy for a variety of diseases. Interestingly, spleen acts an important reservoir during EPC trafficking. Therefore, we investigated the involvement of stromal cell-derived factor-1 (SDF-1)/CXCR4 in EPC settlement in the spleen. EPC were cultured and characterized as previous methods. Then, 1 x 10(6) EPC were labeled with DiI-LDL and intravenously infused into C57/BL6 mice. Immunohistochemical staining showed homing of transplanted EPC in the spleen 24 h later, indicating recruitment of transplanted EPC into the spleen. The distribution of EPC in different organs was evaluated by fluorescence-activated cell sorting of Sca-1/Flk-1(+) cells, which demonstrated settlement of EPC in the spleen. Removal of the splenic niche by splenectomy augmented circulating EPC 12 and 24 h later, indicating an important role of spleen on modulation of EPC-circulating dynamics. Expressions of SDF-1 in the spleen and CXCR4 in EPC were revealed by enzyme-linked immunosorbent assay (ELISA) and reverse transcription polymerase chain reaction (RT-PCR). A modified Boyden chamber assay showed that SDF-1 (10 or 100 ng/mL) induced EPC migration in vitro. Injection of the SDF-1 protein into the spleen increased the number of splenic EPC. In contrast, injection of a SDF-1 antibody or AMD3100 (SDF-1/CXCR4 axis antagonist) attenuated their settlement and did not induce EPC apoptosis. These results indicate that the SDF-1/CXCR4 axis is involved in recruitment of EPC to the spleen, and enhances our understanding of EPC-circulating kinetics.

Inhibitor of DNA binding-1 promotes the migration and proliferation of endothelial progenitor cells in vitro.

Migration and proliferation of endothelial progenitor cells (EPCs) are the key mechanisms in re-endothelialization after vascular injury. Inhibitor of DNA binding-1 (Id1) function has been linked to the proliferation, migration, and senescence of cells, and studies have shed light on the relationship between Id1 and the biological functions of EPCs. On the basis of the available data concerning Id1 and the behavior of EPCs, we hypothesized that Id1 was an important regulator in modulating the migration and proliferation of EPCs. Culture of spleen-derived EPCs was done as previously described. Id1 was presented at low levels in EPCs. Id1 was localized predominantly in the cytoplasm, and was rapidly upregulated by stimulation with serum and vascular endothelial growth factor. The migration and proliferation of EPCs were extensively improved by overexpression of adenovirus-mediated exogenous Id1 and inhibited by silencing of endogenous Id1 in EPCs. These results suggest that Id1 has a direct role in regulation of the migration and proliferation in EPCs.

SDF-1alpha involved in mobilization and recruitment of endothelial progenitor cells after arterial injury in mice.

BACKGROUND: Endothelial progenitor cells (EPCs) can be mobilized by cytokines and recruited to sites of neovascularization and neointima, where they differentiate into mature endothelial cells. It is thought that stromal cell-derived factor-1alpha (SDF-1alpha) is involved in ischemia-mediated mobilization and homing of EPCs and in vascular injury-mediated mobilization and homing of vascular smooth muscle progenitor cells. It is unclear if SDF-1alpha plays a similar role in the mobilization and recruitment of EPCs after vascular injury. METHODS AND RESULTS: SDF-1alpha was detected by reverse transcriptase-polymerase chain reaction and Western blot in the carotid arteries of mice at different times after wire-induced injury. SDF-1alpha expression was evident at 1 day and peaked at 3 days after arterial injury. In an ELISA test, a rise in the plasmatic concentration of SDF-1alpha and a significant reduction of SDF-1alpha bone marrow (BM) concentration were noticed at different times after injury (Days 1, 3, and 7). Fluorescence-activated cell sorting analysis revealed that the amount of circulating EPCs was increased shortly after induction of vascular injury and persisted for up to 7 days. In SDF-1alpha antibody-treated mice, only a small rise in the amount of circulating EPCs was noted at 1 day. En-face microscopy and immunohistochemical analysis showed that systemic injection of EPCs after vascular injury demonstrated their recruitment to the sites of endothelial denudation, where they could adopt an endothelium-like phenotype and accelerate reendothelialization of the injured arteries. Fewer CXCR4 (receptor of SDF-1)-blocked EPCs could home to the sites of endothelial denudation, and accelerated reendothelialization was not observed in this group. Treatment of mice after carotid injury with a neutralizing SDF-1alpha monoclonal antibody for 2 weeks reduced reendothelialization area. CONCLUSION: We demonstrated for the first time that SDF-1alpha plays an important role in reendothelialization after vascular injury in mice. This contribution appears to be attributable to SDF-1alpha-dependent mobilization and recruitment of circulating EPCs.

Young environment reverses the declined activity of aged rat-derived endothelial progenitor cells: involvement of the phosphatidylinositol 3-kinase/Akt signaling pathway.

BACKGROUND: Although age-related impairment of endothelial progenitor cells (EPCs) has been documented in recent studies, the detailed role of aging-induced environment in EPCs remains unclear. METHODS: Two and 20 months old Sprague-Dawley female rats were used in the present study. EPCs isolated from young (YEPCs) and aged (AEPCs) rats were cultured with young or aged serum. EPC migration and proliferation were detected with a modified Boyden chamber and the MTT assay, respectively; EPC differentiation was detected by reverse-transcription polymerase chain reaction or fluorescence-activated cell sorting; Akt and phosphorylated-Akt protein expression was detected with Western blotting. EPC transplantation was performed in the rat carotid artery injury models. RESULTS: Young serum significantly promotes AEPC migration, proliferation, and differentiation and increases phosphatidylinositol 3-kinase (PI3-K) and endothelial nitric oxide synthase activity in AEPCs compared with aged serum; total-Akt and phosphorylated-Akt protein expressions in AEPCs are also significantly upregulated by young serum. Transplanted AEPC numbers at vascular injury sites in the young rat carotid artery injury model significantly increased compared with those in aged models. Those effects could be reasonably attenuated by the PI3-K-specific blocker wortmannin. CONCLUSION: A young environment partly restores the declined AEPC activity and promotes AEPC homing to vascular injury sites; activation of the PI3-K/Akt signaling pathway is at least partly responsible for this process.

Estrogen induces endothelial progenitor cells proliferation and migration by estrogen receptors and PI3K-dependent pathways.

Estrogen induces endothelial progenitor cells (EPCs) migration and proliferation, which may serve as a potential target for coronary artery disease, but the mechanisms are unclear. We hypothesized that estrogen receptors (ERs) and phosphatidylinositol 3-kinase (PI3K) signaling pathway, which represent particularly important roles of action for estrogen, may contribute to estrogen-induced EPCs migration and proliferation. Bone marrow mononuclear cells (MNCs) were cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with growth factors as previously described. A total of 87.32+/-5.13% of adherent cells showed uptake of acetylated low-density lipoprotein and lectin binding. Immunostaining and fluorescence activated cell sorting confirmed the endothelial progenitor phenotype. RT-PCR, immunocytochemistry staining and Western blot demonstrated expression of ERs. Exposure to 17beta-estradiol significantly improved EPCs migration and proliferation. Those effects were blocked by pretreatment with the pharmacological PI3K blockers LY294002 (1 h, 10 micromol/L) and ICI-182780 (1 h, 10 micromol/L), a specific estrogen receptor antagonist, which show involvement of estrogen receptors and PI3K pathway. These results suggest that estrogen induces EPCs migration and proliferation via ERs and PI3K pathway which provided a novel insight and treatment strategy of vascular biology.

[Effects of endothelial lipase on mRNA expression of adhesion molecule of human umbilical vascular endothelial cells].

OBJECTIVE: To explore the relationship between human umbilical vascular endothelial cells (HUVECs) and endothelial lipase (EL), and the effect of EL on expression of endothelial cell adhesion molecule (ICAM). METHODS: HUVECs was treated with tumor necrosis factor-alpha(TNF-alpha) 10 microg/L and the mRNA of adhesion molecules [intercellular adhesion molecule-1 (ICAM-1), vascular cellular adhesion molecule-1 (VCAM-1) and E-selectin] were detected by reverse transcription-polymerase chain reaction (RT-PCR). Then the effect of 50 microg/L anti-endothelial lipase (anti-EL) antibody on the influence of TNF-alpha on these adhesion molecules was observed. RESULTS: After being treated with TNF-alpha, the mRNA of adhesion molecules expressed by HUVECs were significant up-regulated, there was significant difference compared with control group (all P<0.01). These effects of TNF-alpha were significantly abolished by 50 microg/L anti-EL antibody (P<0.05 or P<0.01). CONCLUSION: EL can affect the expression of adhesion molecules on endothelial cell adhesion molecule. This effect of EL may play a role in the pathophysiologic process in the pathogenesis progress of atherosclerosis.

AMD3100 mobilizes endothelial progenitor cells in mice, but inhibits its biological functions by blocking an autocrine/paracrine regulatory loop of stromal cell derived factor-1 in vitro.

Endothelial progenitor cells (EPCs), a CXCR4-bearing cell line, are thought to positively influence reendothelialization, vascular repair, and angiogenesis. AMD3100, a highly selective antagonist of stromal cell derived factor (SDF)-1 that binds to its receptor, CXCR4, has been shown to induce rapid mobilization of hematopoietic stem cells in mice, dogs, and humans. Results of this study indicate that AMD3100 injection can induce a rapid and potent mobilization of EPCs in mice compared with saline injection. The study demonstrates that murine spleen-derived EPCs can produce high levels of SDF-1 in vitro. Blocking this endogenous SDF-1 with AMD3100 decreases the number of EPCs; inhibits the proliferation, migration, and adhesion of EPCs; and induces EPC apoptosis. In addition, AMD3100 inhibits ectogenous SDF-1alpha induced improvement of EPC functions. However, AMD3100 incubation does not change the functions of CXCR4-negative cell line HPDE6. In conclusion, AMD3100 can be regarded as a potent mobilizer of EPCs in mice. EPCs have an autocrine/paracrine SDF-1 loop, and breaking this loop with AMD3100 can inhibit the EPC functions in vitro.

Autologous endothelial progenitor cells transplantation promoting endothelial recovery in mice.

Transplantation of endothelial progenitor cells (EPCs) restores endothelial function. The present study was designed to determine the effect of autologous EPCs transplantation on the regeneration of endothelium in mice. Mice splenectomy was performed 14 days before carotid artery injury, and mononuclear cells were isolated and cultured in endothelial growth media for 7 days. EPCs were confirmed by immunostaining (CD31, endothelial nitric oxide synthase (eNOS) and double positive for 1,1'dioctadecyl-3,3,3',3-tetramethylindocarbocyanine (DiI)-low-density lipoprotein and ulex europaeus agglutinin (UEA)). Cell counts and fluorescence-activated cell sorting for stem cell marker were performed. 1 x 10(6) 4-,6-Diamidino-2-phenylindole- labeled EPCs or saline were injected through tail vein after wire injury. Two weeks after transplantation, cell tracking and immunohistochemical staining showed homing and incorporation of labeled EPCs in injury artery. Administration of EPCs enhanced reendothelialization (P < 0.05) after 1 week and inhibition of neointima formation at 3 weeks compared with that of saline (P < 0.05, n = 6). These data demonstrate that delivery of autologous EPCs is associated with accelerated reendothelialization and reduced neointimal formation. Thus, delivery of autologous EPCs represents an important vasculoprotective approach to attenuate the response to acute vascular injury.

[New method of left ventricular intubation in anaesthetised rats].

AIM: To search for a new method of left ventricular intubation in rat. METHODS: The wire of percutaneous transluminal coronary angioplasty (PTCA) was put into carotid artery through external carotid artery. Then supported by guide wire, the PE50 tube was advanced into left ventricle. RESULTS: Left ventricular intubation with PTCA guide wire could be performed in 30 rats and successfully repeated in 27 animals. CONCLUSION: The new left ventricular intubation technology in rats is simple and provides a reproducible method.