Abstract:Mitochondrial dysfunction can lead to ATP decrease and reactive oxygen species increase in cells. Therefore, mitochondrial dysfunction is considered to be one of the culprit factors of vascular endothelial cell injury. Many causes are related to mitochondrial dysfunction including mitochondrial DNA mutations, mitochondrial fusion and fission imbalance, and mitophagy dysfunction. This review discussed the regulation mechanisms of mitochondrial quality control and mitochondrial dysfunction in vascular endothelial cell injury, which provide new ideas for the effective prevention and treatment of atherosclerosis.

Abstract:Coronary artery endothelial injury is the initiating and the most critical factor of atherogenesis. For a long time, researchers have focused on the mechanism of endothelial injury induced by oxidized low density lipoprotein(ox-LDL). With the development of new technologies and methods, the role of micro-RNA (miRNA) in the process of endothelial cell injury induced by ox-LDL has been gradually discovered. This review briefly describes the miRNAs involved in endothelial injury such as endothelial inflammation, autophagy, apoptosis and dysfunction under the condition of hyperlipidemia. Summarizing these miRNAs may permit new ideas for the prediction, diagnosis and even treatment of coronary atherosclerosis.

Abstract:Aim To investigate whether microRNA-20a-5p (miR-20a-5p) alleviates oxidized low density lipoprotein (ox-LDL)-induced injury of human umbilical vein endothelial cells (HUVEC) by targeting myocardin-related transcription factor A (MRTFA). Methods RT-qPCR was used to detect the expression of miR-20a-5p in HUVEC induced by ox-LDL of various doses at different time. MTT, flow cytometry and Western blot assays were performed to evaluate the effect of overexpression of miR-20a-5p and MRTFA on the ox-LDL-induced proliferation and apoptosis of HUVEC.Lactate dehydrogenase (LDH) kit was conducted to determine the effect of overexpression of miR-20a-5p on ox-LDL-induced LDH release in HUVEC. ELISA assay was employed to examine the effects of upregulation of miR-20a-5p and MRFA on ox-LDL-mediated changes of oxidative stress indexes superoxide dismutase (SOD), nitric oxide (NO), endothelial nitric oxide synthasee (eNOS) and malondialdehyde (MDA) in HUVEC. Luciferase reporter Western blot assays was introduced to validate the relationship between miR-20a-5p and MRTFA. Results The expression of miR-20a-5p was significantly decreased in a time or dose dependent manner. Overexpression of miR-20a-5p attenuated the effect of ox-LDL on proliferation, apoptosis, and LDH release in HUVEC. Upregulation of miR-20a-5p repaired ox-LDL-induced oxidative stress injury in HUVEC. MRTFA was a direct target gene of miR-20a-5p. MRTFA overexpression undermined the effects of miR-20a-5p on proliferation, apoptosis, and oxidative stress injury index in ox-LDL-treated HUVEC. Conclusion miR-20a-5p can repair ox-LDL-induced HUVEC damage via targeting MRTFA.

Abstract:Aim To investigate the antagonistic effect of endostatin (ENDO)-vascular endothelial growth inhibitor (VEGI) recombinant adenoviruses to the vascular endothelial cell injury caused by homocysteine (Hcy). Methods The Ad-hENDO-VEGI151 from the fusion protein of ENDO and VEGI was used to transfect the human ECV304 caused by Hcy. The expression of fusion protein was detected by Western blot, the leakage of lactate dehydrogenase (LDH) was detected by automatic biochemical analyzer, the cell viability was detected by trypan-blue staining method, and the expression of tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1) were detected by ELISA. Results The transgenic efficiency of recombinant adenovirus was relatively high. A fusion protein with molecular weight of 41 kDa was expressed in the Ad-hENDO-VEGI151 recombinant adenovirus of ECV304 cells. Hcy (0.1~1.0 mmol/L) increased the leakage of LDH and decreased the cell viability in concentration-dependent manner. The recombinant adenovirus effectively inhibited the injury of Hcy on human vascular endothelial cells (P＜0.05). Conclusion The ENDO-VEGI recombinant adenoviruses had antagonistic effect on vascular endothelial cell injury caused by Hcy, which might provide an idea for future prospecting.

Abstract:Atherosclerosis is the pathological basis of cardiovascular and cerebrovascular diseases. Chronic inflammatory reaction and endothelial dysfunction play an important role in the occurrence and development of atherosclerosis. In recent years, some new markers of endothelial injury and inflammation have been identified, including Endoglin (CD105), Endocan, Apelin, and chemokines. This article mainly introduces the role of Endoglin in atherosclerosis.

Abstract:With the accelerated aging of society, the incidence of atherosclerosis(As) is increasing year by year. Now that the initial event of the atherosclerosis is endothelial damage, while lipid metabolism is a major risk factor for vascular injury. But now research shows that some non-lipid material also play an important role in the development of As, such as high homocysteine (HHCy), high blood sugar and high uric acid. These non-lipid factors play a major role in vascular endothelial cells, interference by expression of sticky molecule, changing the state of the pathophysiology of endothelial cells, leading to endothelial damage, contributing to the formation of As lesions. This paper describes some of the mechanisms that the changes of adhesion molecules in non-lipid factors induced atherosclerotic vascular endothelial injury, and describes some of the therapeutic intervention targets expression of adhesion molecules, which has important clinical significance for the treatment of atherosclerosis leading to coronary heart disease, myocardial infarction and other cardiovascular diseases.

Abstract:Endothelial cells are considered as important organs for metabolism and secretion, and play an importmant role in regulating the function of blood vessel. The development of multiple cardio-cerebrovascular diseases, such as atherosclerosis, hypertension and diabetic vascular complications, is closely related to endothelial injury. The mechanisms of vascular endothelial cell injury have not yet fully clarified. A large number of studies have shown that mechanisms of endothelial cell injury are mainly related to inflammatory reaction and oxidative stress. Endothelial progenitor cells play an important role in repairing endothelial injury. A variety of chemical drugs and traditional Chinese medicine play the role of endothelial protection by means of reducing induced factors, inhibiting inflammation reaction and oxidative stress, delaying endothelial cell aging and other ways.

Abstract:Aim To study the effect of Xuefuzhuyu capsule on thrombelastography (TEG) in rats with vascular endothelial injury induced by homocysteine (Hcy). Methods SD rats were randomly divided into 6 groups:normal group, model group, Tongxinluo capsule 0.21 g/kg group, Xuefuzhuyu capsule 1.6,0.8 and 0.4 g/kg groups. Rat endothelial injury models were established by intragastric gavaged of methionine once per day for continuous 4 weeks. Meanwhile, each treated group was intragastric gavaged of corresponding drug. After 4 weeks, serum levels of Hcy and endothelin-1 (ET-1), plasma level of nitric oxide (NO), platelet (PLT) number and mean platelet volume (MPV), as well as TEG were detected. Results All doses of Xuefuzhuyu capsule could significantly reduce the serum levels of Hcy and ET-1(P＜0.01), increase the plasma level of NO and MPV, and lower the number of PLT number, with statistical significances in 0.8 g/kg group (P＜0.05). All doses of Xuefuzhuyu capsule could significantly reduce MA (P＜0.01), the R of 1.6 and 0.8 g/kg groups were significantly prolonged (P＜0.01 or P＜0.05 ), the Angle of 0.8 g/kg group showed significant decrease (P＜0.01). Conclusion Xuefuzhuyu capsule can relieve the state of platelet hyper function and high coagulation factor, and attenuate high Hcy induced injury in rats.

Abstract:Aim To develop a rabbit model of vulnerable atherosclerotic plaque by cryogenic gas-induced endothelial injury combined with high-fat diet. Methods 24 healthy male New Zealand rabbits （3 months） were randomly divided into three groups: control blank group （group A）, sham-operated group （group B） and temperature control gas injury group （group C） with 8 in each group. After one week high-fat diet, the rabbits in group C were underwent carotid artery intima injury using cryogenic gas. The rabbits in group B suffered surgical operations without cryogenic gas. After the operation, the rabbits in group B and group C were kept feeding on high-fat diet for 12 weeks, whereas the ones in group A were kept on normal diet. All rabbits were killed after 13 weeks. Then paraffin-embedded and frozen sections were used for HE staining, Masson trichrome staining and elastic fiber staining and oil red O staining to analyze the changes of vascular morphology. Additionally, rat anti-rabbit macrophage antibody 11 （RAM11） monoclonal antibody was applied for animal immunohistochemistry staining. Results The rabbit carotid atherosclerosis established in our study was in line with the progress characteristics of vulnerable plaque, involving thin fibrous cap, large lipid core and macrophages and foam cells in the intima as well as endothelial cells shedding or local small scattered thrombosis. The rabbit carotid in sham-operated group showed intimal hyperplasia and partly showed small primary plaques infiltrated by macrophages, which was in line with the change of fatty streaks phase. There is no plaque visible in the control blank group. Conclusion It is viable and easy to develop a rabbit model of typical vulnerable atherosclerotic plaque by injuring carotid intima with temperature control gas combined with high-fat diet.

Abstract:Aim To investigate the effect of estradiol on inhibition of neointimal proliferation after rat carotid artery balloon injury. Methods Eight-ten week-old S-D rats were divided into intact control group (n=7), gonadectomized control group (n=7) and estradiol (n=7,gonadectomization)group in each sex. Left carotid artery was not injured with 2.0F PTCA balloon until estradiol had been injected for three days. Rats were killed after injury two weeks later. Neointimal areas, ratios of intimal areas and media areas were measured with computer. Results Neointimal areas and ratios of inttimal areas and media areas in male in estradiol group were significantly less than those in intact control group (allP<0.01), and in gonadectomized control group (allP<0.05). Those in female ,in estradiol group were less than those in godectomized control group evidently (allP<0.01),were also similar to those in intact control group (all P>0.05). Conclusion Estradiol inhibited neointimal proliferation after the gonadectomized rat carotid artery balloon injury.