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1.
Endothelial cells are the cells lining the inner surfaces of blood vessels. They build up a single cell layer and play an important role in the regulation of vascular functions and the maintenance of homeostasis. The activation or injury of endothelial cells is associated with multiple diseases, including hypertension, atherosclerosis, cancer, diabetes, etc. Recent studies have found that microparticles are involved in the process of endothelial cell injury, thus playing a part in the development of many diseases. miRNAs enfolded in the microparticles have become importance in recent years. Moreover, recent studies also found that the concentration of the miRNAs enfolded in the microvesicles is higher than that of the miRNAs in the plasma, which means that the microparticles are the main form of miRNAs present in peripheral circulatory system. This article is to review the recent research progress in microparticle-encapsulated miRNAs and their regulatory effect on endothelial cell injury.  相似文献   

2.
The vascular endothelial progenitor cells are a population of functional endothelial precursors in circulating blood, which are derived from bone marrow or cord blood. CD34+, Flk-1+ and ACl33+ are their molecular markers. In this review, the functional characterization of vascular endothelial progenitor cells is introduced and the relationship between vascular endothelial progenitor cells and angiogenesis in is chemic cardiovascular diseases is discussed. These data may offer a foundation for the development of therapeutic angiogenesis for the prevention and treatment of ischemic cardiovascular diseases by transplantation of vascular endothelial progenitor cells.  相似文献   

3.
AIM To investigate the role of monocyte chemoattractant protein-1 (MCP-1) and its receptor CC chemokine receptor 2 (CCR2) in ethanol-promoted breast cancer angiogenesis and the underlying mechanism. METH?ODS: A mouse model of transplanted breast tumor with moderate alcohol consumption was established. The correlations between the expression of MCP-1/CCR2 and the expression of angiogenesis markers [platelet endothelial cell adhesion molecule-1 (PECAM-1) and vascular endothelial growth factor (VEGF)] in tumor tissues were examined by immunohistochemistry. In vitro, a 3D tumor-endothelial co-culture system was established to observe tumor angiogenesis and the role of MCP-1/CCR2 signaling pathway in alcohol-mediated angiogenesis. The cell migration ability was detected to clarify whether MCP-1/CCR2 enhanced cell mobility to form new vessels. RESULTS MCP-1 and CCR2 were both highly expressed in the breast tumor tissues of tumor-bearing mice consuming alcohol, and their expression levels were consistent with the angiogenic markers PECAM-1 and VEGF (P<0.05). The interaction between mouse breast cancer E0771 cells and endothelial cells was observed to promote angiogenesis in the 3D tumor-endothelial co-culture system with or without alcohol stimulation. MCP-1 promoted this kind of tumor angiogenesis, while CCR2 antagonist effectively inhibited the tumor angiogenesis and especially blocked alcohol-induced angiogenesis. Activation of MCP-1/CCR2 signaling pathway enhanced the migration ability of endothelial cells. CONCLUSION The MCP-1/CCR2 signaling pathway plays an important role in promoting the angiogenesis of breast cancer stimulated by alcohol. The mechanism might be that MCP-1 improves the migration of endothelial cells and then promotes angiogenesis.  相似文献   

4.
Atherosclerosis (AS) is a common cardiovascular disease and a major cause of coronary heart di-sease, cerebral infarction and peripheral vascular disease. Circular RNA (circRNA) is a class of circularly closed non-co-ding RNAs that play an important role in the formation of AS. Physiological and pathological significances of the processes such as lipid metabolism, endothelial cell damage, vascular smooth muscle cell proliferation and migration, monocyte pha-gocytosis and foam-like cell formation, and inflammatory responses are involved in the development of AS. Most circRNA adjust mRNA expression by regulating microRNAs (miRNAs). circRNA provides new ideas and targets for the diagnosis and treatment of AS.  相似文献   

5.
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6.
AIM: To establish a three-dimensional angiogenesis model in vitro for observing the influence of tumor cells on angiogenesis, and to explore its possible molecular mechanism. METHODS: Human umbilical vein endothelial cells (HUVECs) and mouse endothelial cells SVEC4-10EE2 were coated on the surface of beads, and then mixed with fibrinogen and seeded in cell culture plates containing thrombin. The cultured endothelial cells coated on the beads grew into a vessel-like structure in a three-dimensional space containing fibrin condensate to establish an in vitro three-dimensional angiogenesis model. Tumor cells MDA-MB-231 and E0771 were co-cultured in the model to observe the effect of tumor cells on angiogenesis in vitro,respectively. The concentrations of monocyte chemoattractant protein-1 (MCP-1) and vascular endothelial growth factor (VEGF) in the tumor cells culture supernatant were measured by ELISA. An antagonist of CCR2 (receptor of MCP-1), along with SU5416 (an inhibitor of VEGF receptor), were added to the tumor cell co-culture system. The supernatant of the tumor cells was collected as a conditioned medium, which was then added to the angiogenesis system of HUVECs or SVEC4-10EE2 cultured individually. The effect of conditioned medium on angiogenesis was observed under the conditions of with or without SU5416, as well as with or without CCR2 antagonist. RESULTS: Under normal condition, HUVECs and SVEC4-10EE2 formed a multi-cellular vascular structure the three-dimensional angiogenesis model in vitro. The co-culture of MDA-MB-231 (E0771) cells significantly promoted in the formation of membrane-like structures. The ELISA results showed that the levels of MCP-1 and VEGF in the supernatant of tumor cells were significantly elevated (P<0.05). MCP-1 promoted the formation of membrane tube in three-dimensional culture system in vitro. After adding the antagonists of MCP-1 receptor CCR2 and VEGF (SU5416), the angiogenesis was significantly inhibited (P<0.05). At the same time, conditioned medium promoted the formation of extracorporeal membranes in the endothelial cells. The promoting effect was blocked by CCR2 antagonists and SU5416 (P<0.05). CONCLUSION: The in vitro three-dimensional angiogenesis model is successfully established. Tumor cells significantly promote the formation of membrane tubes. The effect of tumor cells might be related to MCP-1 and VEGF secretion.  相似文献   

7.
LIU Ji-yan  WEI Yu-quan 《园艺学报》2004,20(7):1309-1313
Angiogenesis, or the formation of new blood vessels out of pre-existing capillaries, is very important in many physiologic and pathologic processes, such as embryonic development, cancer, retinopathies, etc. Vascular endothelial growth factor receptor-2 (VEGFR-2) plays a key role in angiogenesis. In this review, we discussed the structure, function and signal transduction of vascular endothelial growth factor receptor-2. Understanding these should provide important insights into how new strategies can be devised to interfere in the physiologic and pathologic processes involved in angiogensis.  相似文献   

8.
ATM: To explore the molecular mechanism that curcumin inhibits hepatocyte growth factor (HGF) induced angiogenesis. METHODS: The effects of curcumin, c-Met inhibitor SU11274, phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 and mTOR inhibitor rapamycin on HGF-induced endothelial cell migration, tubule formation ability, vascular endothelial growth factor (VEGF) expression, related signaling pathways and the density of blood vessels in tumors were observed by the methods of capillary forming experiments, wound healing assay, Western blot and animal study. RESULTS: SU11274, LY294002, rapamycin and curcumin significantly inhibited HGF induced endothelial cell migration, tubule formation and VEGF expression, suppressed the phosphorylation of c-Met/AKT/mTOR/S6 pathway related molecules, reduced VEGF expression and microvascular density in the tumors. CONCLUSION: Curcumin inhibits HGF induced angiogenesis by inhibiting c-Met/AKT/mTOR/S6 pathway activation.  相似文献   

9.
MO Qian  LI Dan  LING Wen-hua 《园艺学报》2012,28(7):1187-1191
AIM: To study the effect of miR-18a on angiogenesis of human aortic artery endothelial cells. METHODS: After 10 nmol/L miR-18a mimics or 20 nmol/L inhibitor was transfected into human aortic endothelial cells, the expression level of miR-18a was determined by qRT-PCR, and the capacities of endothelial cell angiogenesis, such as migration, adhesion and tube formation, were observed. RESULTS: Forty-eight hours after transfection with miR-18a mimics, the expression of miR-18a was as 608 folds as the control (P<0.05), but decreased to 31% of the control level in miR-18a inhibitor transfection group (P<0.05). Compared with control group, the numbers of endothelial cells, which migrated to the lower Transwell chamber and formed capillary-like tubes, declined by 60% and 52%, respectively, in miR-18a mimics group (P<0.01), and they increased by 100% and 84%, respectively, in miR-18a inhibitor transfection group (P<0.05, P<0.01). In addition, the inhibitor treatment group displayed more potent adhesion capacity, 43% higher than that in control group (P<0.05). CONCLUSION: miR-18a is involved in angiogenesis of human arterial endothelial cells, and might be a potential molecular therapeutic target of vascular diseases.  相似文献   

10.
AIM: To investigate the therapeutic action of secreted endostatin (ES) on breast cancer cells. METHODS: Retroviral-mediated endostatin gene was transferred to breast cancer cell line MDA-MB-231. The ES biological properties and function were evaluated by polymerase chain reaction (PCR), MTT and a murine xenograft model. RESULTS: After retroviral transduction, endostatin genetically modified breast tumor cells were confirmed by PCR, and the integration and durative expression of endostatin gene was successfully committed. Compared with controls, endostatin secreted by genetically modified cells markedly inhibited endothelial cell proliferation (P<0.05) while the influences on the growth of MDA-MB-231 cell line in vitro were not found (P>0.05). The results of the transplanted subcutaneous tumor model in nude mice suggested that the subcutaneous growth of MDA-MB-231 was significantly inhibited by the expression of endostatin gene (P<0.05). In experimental groups, the tumor microvascular density (MVD) and VEGF expression were decreased. CONCLUSION: Retroviral- mediated overexpression of endostatin inhibits the proliferation of vascular endothelial cells and angiogenesis that associated with tumor growth in vivo via the paracrine pathway, which has a potential effect in the angiostatic gene therapy for breast cancer.  相似文献   

11.
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12.
As an important organ in the body, blood vessels transport oxygen and nutrients to the tissues of the body. Endothelial cells are layers of cells lined with blood vessels whose metabolism is involved in regulating multiple links of vascular development and vascular diseases. Glucose metabolism provides the main energy for endothelial cells, and changes in glucose metabolism regulation affect vascular development and even lead to various diseases. Recently, strategies have been proposed to target endothelial cell metabolism for the treatment of vascular diseases. This article reviews the role of endothelial cell glucose metabolism in vascular development and vascular diseases in recent years.  相似文献   

13.
AIM: To investigate the differentiation potential of human placenta derived mesenchymal stem cells (PDMSCs) into endothelial cells (ECs) in vitro. METHODS: PDMSCs were isolated from human placenta tissues, characterized by flow cytometry and induced to differentiate into endothelial cells with 50 μg/L VEGF and 10 μg/L bFGF. To detect the specific markers of ECs during the process of differentiation, the method of immunocytochemistry was performed. The specific structure and function of endothelial cells were observed by transmission electron microscopy and in vitro angiogenesis assay kit, respectively. RESULTS: CD105 and CD106 were positive in PDMSCs, while CD34,CD45 and CD31 were negative.The ECs differentiated from PDMSCs showed cobblestone-like morphology, and expressed early endothelial marker of Flk-1/KDR and mature endothelial markers of CD31, vWF and CD144/VE-cadherin in a time-dependent manner during the endothelial cell differentiation (0 day, 4 days, 8 days and 12 days). The endothelial specific structure, Weibel-palade body, was observed under transmission electron microscope. The inoculation of ECs on the extra cellular matrix gel formed capillary-like structures. CONCLUSION: Plentiful PDMSCs can be isolated from placenta, and differentiate into the cells with functional characteristics of ECs in vitro, indicating that the placenta tissues will become optimal source of seed cells for vascular engineering and regenerative medicine.  相似文献   

14.
AIM:The current study was designed to construct eukaryotic expression vector containing NK4 gene and transfect it into human pancreatic cancer cell lines.METHODS:The recombinant of pcDNA3/hNK4 was digested by restriction enzyme,the NK4 gene was cloned into a high effective eukaryotic expressing plasmid which contains CMV2 immediate early gene promoter and then transiently introduced into the pancreatic cancer cell line SW1990 by lipo fectamine and clonal cel lines that secrete high levels of NK4 protein were isolated.The expression of NK4 was observed by RT-PCR and Western blot,in vitro the vascular endothelial cell proliferation inhibiting activity of NK4 was examined by 3-[4,5-dimethylthiazolzyl]-2,5-diphenyl tetrazolium bromide(MTT)method.RESULTS:A specific expression of NK4 gene mRNA by lipofectamine-mediated transfer exhibited only in SW1990/NK4 cells,Western blot analysis demonstrated that there was positive expression of NK4 protein(50 kD).The NK4 inhibited proliferation of the vascular endothelial cellsin vitro.CONCLUSION:The recombinant of pRC/CMV2-hNK4 is a high effective expressing eukaryotic vector.The bio-engineering product of the NK4 is an angiogenesis inhibitor and may play an important role in the gene therapy for tumor.  相似文献   

15.
Endothelial progenitor cell (EPC) is a kind of directional cell that is able to differentiate to endothelial cell. The role of EPC is associated not only with vasculogenesis during embryonic development but also with physiological organ maintenance and angiogenesis during postnatal and adult period. There is a good clinical therapeutic prospective use for EPC in the treatment of ischemia diseases and inhibition of tumor angiogenesis.  相似文献   

16.
AIM: To evaluate the effect of microRNA-155(miRNA-155) on the regulation of angiogenesis in diabetic rats with cerebral ischemic injury. METHODS: Adult male Sprague-Dawley rats were randomly divided into 5 groups:sham group, cerebral ischemia group, diabetic cerebral ischemia group, diabetic cerebral ischemia+miRNA-155 inhibitors group and diabetic cerebral ischemia+scramble group. Diabetes model was made by injection of streptozocin and permanent cerebral ischemic model was developed by suture-occluded method. The scores of neurological deficit and infarct volume were estimated at 24 h after cerebral ischemia. miRNA-155 level was detected by real-time polymerase chain reaction. The expression of platelet endothelial cell adhesion molecule-1(PECAM-1/CD31) and vascular endothelial growth factor(VEGF) was detected by Western blotting. RESULTS: miRNA-155 inhibitor significantly reduced miRNA-155 levels in the ischemic cortex(P<0.05), improved the scores of neurological deficit, reduced infarction size and upregulated the levels of CD31 and VEGF(P<0.05). CONCLUSION: miRNA-155 has a critical role in the regulation of angiogenesis in diabetic rats with cerebral ischemia. Down-regulation of miRNA-155 using miRNA-155 inhibitor attenuates brain infarct injury in diabetic rats.  相似文献   

17.
AIM: To observe the effects of microparticles derived from bone marrow mesenchymal stem cells (MSC-MPs) on angiogenesis and cardiac function in a rat myocardial infarction model. METHODS: MSCs were obtained from Sprague-Dawley rats. MSCs were treated under serum-free condition in hypoxia for 72 h, and the microparticles were isolated from the supernatants. The phenotypic profile of MSC-MPs was determined by bead-based flow cytometry and the morphology was observed under a transmission electron microscope. The rat myocardial infarction model was established. The cardiac function was evaluated by echocardiography after the intramyocardial injection of MSC-MPs. The myocardial infarct size was observed by Masson staining. The blood vessel density in the peri-infarcted area was measured using immunohistochemical staining for von Willebrand factor and α-smooth muscle actin. The expression of vascular endothelial growth factor (VEGF) was analyzed by real-time PCR. RESULTS: Apoptotic MSCs released a large quantity of microparticles which were phenotypically similar to the parent MSCs and 100~1 000 nm in diameter. The cardiac functions of myocardial infarction rat model were improved at 7 d and 28 d after intramyocardial injection of MSC-MPs compared with control group. The myocardial infarct size was reduced and angiogenesis was promoted significantly in the infarcted heart injected with MSC-MPs 28 d after treatment. MSC-MPs treatment also increased the expression level of VEGF within 7 d.CONCLUSION: MSC-MPs protect cardiac tissue from ischemic injury and improve cardiac function by promoting angiogenesis after myocardial infarction.  相似文献   

18.
AIM: To investigate the influence of GM-CSF on human vascular endothelial cells induced to form new blood vessels and the role of VEGF. METHODS: HUVECs were cultured by Matrigel to set up a stable angiogenesis system with the stimulating factors. The rhGM-CSF concentration-dependent and time-dependent effects and the role of VEGF165 were detected. CD34 was measured by immunochemical staining and numbers of vessel formation was calculated under microscopic observation. RESULTS: After treatment with rhGM-CSF at various concentrations and at different time points, the numbers of vessel formation increased in a dose-dependent and time-dependent manner. In the presence of VEGF165, the numbers of vessel formation increased evidently. CONCLUSION: HUVECs were induced to develop tubular structure in vitro cultured with Matrigel. GM-CSF promotes human vascular endothelial cells to form vessel-like structure in vitro in a dose-dependent and time-dependent manner. VEGF also in vitro promotes human vascular endothelial cells to form new vessel-like structure.  相似文献   

19.
AIM: To explore the effect of protein kinase D1 (PKD1) on promoting angiogenesis in vitro and in vivo, and to furnish a new idea on targeting PKD1 for the treatment of ischemic heart disease such as myocardial infarction. METHODS: The culture, isolation and identification of endothelial progenitor cells (EPCs) were performed in vitro. The effects of PKD1 and its specific blocking agent CID755673 on expression levels of vascular endothelial growth factor (VEGF) and kinase insert domain receptor (KDR) in EPCs were determined. The rat model of myocardial infarction was established, the intervention effects of PKD1 and CID755673 on morphology, changes of microvessels and endothelial cells, and the expression of VEGF and KDR in the impaired myocardial tissue were analyzed. RESULTS: PKD1 significantly upregulated the expression of VEGF and KDR in EPCs in vitro. Meanwhile, the structure of myocardial tissue was more regular and clear, the cytomembrane of endothelial cells were more smooth and integrity, the pericytes were visible, and the expression of VEGF and KDR was significantly increased in PKD1 treatment group in vivo.CONCLUSION: PKD1 has the ability of angiogenesis obviously, which might be mediated by VEGF.  相似文献   

20.
AIM: To investigate whether and how N, N-dimethylsphingosine (DMS) plays a role in modulating the adhesion of monocytes to vascular endothelial cells, and identify whether human umbilical vein endothelial cell line EA.hy926 take place of the vascular endothelial cells.METHODS: Adhesion ratio was measured by flow cytometry, and immunohistochemistry was used to detect the expression of ICAM-1 and P-selectin in HUVEC: EA.hy926 cells after the effect of DMS. RESULTS: DMS inhibited the adhesion of monocytes to HUVEC: EA.hy926 cells in a time-dependent and concentration-dependent manner by reducing the expression of ICAM-1 and P-selectin. CONCLUSIONS: DMS reduced adhesion molecule expression in vascular endothelial cells. DMS may be an important contributor to reduce adhesion ratio, suggesting that DMS plays a negative role in proinflammatory and immune functions of the modified vascular endothelial cells during atherosclerosis and restenosis.  相似文献   

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