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| 1 | Expression of vascular endothelial growth factor and its role in oncogenesis of human gastric carcinoma显示文摘AIM To establish the role of vascular endothelial growth factor (VEGF) in the oncogenesisof human gastric carcinoma more directly.METHODS The expression of VEGF and its receptor kinase-domain insert containing receptor (KDR) in human gastric cancer tissue were observed by immunohistochemical staining. VEGF levels were manipulated in human gastric cancer cell using eukaryotic expression constructs designed to express the complete VEGF165 complimentary DNA in either the sense or antisense orientation. The biological changes of the cells were observed in which VEGF was up-regulated or downregulated.RESULTS VEGF-positive rate was 50%, and VEGF was mainly localized in the cytoplasm and membrane of the tumor cells, while KDR was mainly located in the membrane of vascular endothelial cells in gastric cancer tissues and peri-cancerous tissue. In 2 cases of 50 specimens, the gastric cancer cells expressed KDR,localized in both the cytoplasm and membrane.Introduction of VEGF165 antisense into human gastric cancer cells ( SGC-7901, immunofluorescence intensity,31.6%)) resulted in a significant reduction in VEGFspecific messenger RNA and total and cell surface VEGF protein ( immunofluorescence intensity, 8.9%)(P<0.05). Conversely, stable integration of VEGF165 in the sense orientation resulted in an increase in cellular and cell surface VEGF (immunofluorescence intensity,75.4%) (P<0.05). Lowered VEGF levels were associated with a marked decrease in the growth of nude mouse xenografted tumor (at 33 days postimplantation, tomor volume: 345.40 ± 136.31 mm3) (P<0.05 vs control SGC7901 group: 1534.40 ± 362.88 mm3), whereas up-regulation of VEGF resulted in increased xenografted tumor size (at 33 days postimplantation, tomor volume: 2350.50 ± 637.70mm3) (P<0.05 vs control SGC-7901 group).CONCLUSION This study provides direct evidence that VEGF plays an important role in the oncogenesis of human gastric cancer. | Du-Hu Liu Xue-Yong Zhang Dai-Ming Fan Yu-Xin Huang Jin-Shan Zhang Wei-Quan Huang Yuan-Qiang Zhang Qing-Sheng Huang Wen-Yu Ma Yu-Bo Chai Ming Jin Institute of Digestive Disease,Xijing Hospital,~2 Department of Gastroenterology,Tangdu Hospital,~3Department of Histology and Embryology,~4 Department of Microbiology,~5 Department of Biochemistry,Fourth Military Medical University,Xi’an 710033,Shaanxi Province,China | 2001 | World Journal of Gastroenterology2001，7，4： | 37 |
| 2 | Expression of CXC chemokine IP-10 in patients with chronic hepatitis B显示文摘BACKGROUND: Chemokines have strong chemoattractant effects and are involved in a variety of immune and inflammatory reactions, such as attracting activated T lymphocytes, neutrophils, monocytes and natural killer cells via the pathway of G protein-coupled receptors to sites of inflammatory injury and contribute to wound repair. This investigation was designed to assess the levels of chemokine interferon-γ inducible protein-10 (IP-10) and IP-10 mRNA, and the relationship between IP-10 mRNA and HBV-DNA and alanine aminotransferase (ALT) in patients with chronic hepatitis B. METHODS: The levels of IP-10 mRNA in peripheral blood mononuclear cells (PBMCs) were kinetically detected by real-time polymerase chain reaction (PCR). The rate of chemokine/GAPDH was regarded as the extreme level of chemokine. The level of IP-10 in serum was measured by enzyme linked immunosorbent assay (ELISA), and the expression of IP-10 in hepatic biopsy tissue was detected by streptavidin-peroxidase (SP) immunohistochemistry. RESULTS: The level of IP-10 mRNA in the PBMCs of patients was 0.7387±0.0768 (lg cDNA/lg GAPDH); it was significantly higher in patients with chronic hepatitis B than that in normal controls (P<0.001). The level of IP-10 in the serum of patients was 660.9±75.5 pg/ml. There was a significant difference between patients with chronic hepatitis B and normal controls (P<0.05). In patients with chronic hepatitis B, the level of IP-10 mRNA in PBMCs was correlated with the IP-10 plasma level(r=0.7312, P<0.001), and the IP-10 plasma level was fairly correlated with the levels of ALT and HBV-DNA plasma (r=0.7235, P<0.001; r=0.7371, P<0.001). IP-10 was found by immunohistochemical analysis to be selectively upregulated on sinusoidal endothelium. CONCLUSIONS: The expression of IP-10 mRNA in PBMCs, IP-10 plasma concentration and the expression of IP-10 in sinusoidal endothelium are all high in patients with chronic hepatitis B. Chemokine IP-10 may play an important role in trafficking inflammatory cells to the local focus in the liver and induce the development of the chronicity of hepatitis B. | Wang, Jian Zhao, Jin-Hong Wang, Ping-Ping Xiang, Gui-Ju | 2008 | Hepatobiliary & Pancreatic Diseases International2008，7，1： | 36 |
| 3 | Reduction of tumorigenicity of SMMC-7721 hepatoma cells by vascular endothelial growth factor antisense gene therapy显示文摘AIM To test the hypothesis to block VEGFexpression of SMMC-7721 hepatoma cells mayinhibit tumor growth using the rat hepatomamodel.METHODS Amplifiy the 200 VEGF cDNAfragment and insert it into human U6 genecassette in the reverse orientation transcribingsmall antisense RNA which could specificallyinteract with VEGF165, and VEGF121 mRNA.Construct the retroviral vector containing thisantisense VEGF U6 cassette and package thereplication-deficient recombinant retrovirus.SMMC-7721 cells were transduced with thesevirus and positive clones were selected withG418. PCR and Southern blot analysis wereperformed to determine if U6 cassette integratedinto the genomic DNA of positive clone.Transfected tumor cells were evaluated for RNAexpression by ribonuclease protection assays.The VEGF protein in the supernatant of parentaltumor cells and genetically modified tumor cellswas determined with ELISA. In vitro and in vivogrowth properties of antisense VEGF cell clonein nude mice were analyzed.RESULTS Restriction enzyme digestion andPCR sequencing verified that the antisense VEGFRNA retroviral vector was successfullyconstructed. After G418 selection, resistantSMMC-7721 cell clone was picked up. PCR andSouthern blot analysis suggested that U6cassette was integrated into the cell genomicDNA. Stable SMMC-7721 cell clone transducedwith U6 antisense RNA cassette could express200bp small antisense VEGF RNA and secretereduced levels of VEGF in culture condition.Production of VEGF by antisense transgeneexpressing cells was 65 ± 10 ng / L per 106 cells,420 ± 45 ng/L per 106 cells in sense group and 485± 30 ng/L per 106 cells in the negative control group, (P<0.05). The antisense-VEGF cell clone appeared phenotypically indistinguishable from SMMC-7721 cells and SMMC-7721 cells transfected sense VEGF. The growth rate of the antisense-VEGF cell clone was the same as the control cells. When S. C. was implanted into nude mice, growth of antisense-VEGF cell lines was greatly inhibited compared with control cells.CONCLUSION Expression of antisense VEGFRNA in SMMC-7721 cells could decrease thetumorigenicity, and antisense-VEGF genetherapy may be an adjuvant treatment forhepatoma. | Yu Cheng Tang Yu Li Guan Xiang Qian Department of Biochemistry, Shanghai Second Medical University, Shanghai 200025, China | 2001 | World Journal of Gastroenterology2001，7，1： | 33 |
| 4 | Vascular endothelial dysfunction, cardiomyopathy a major mediator in diabetic cardiomyopathy显示文摘Diabetes mellitus is currently a major public health problem.A common complication of diabetes is cardiac dysfunction,which is recognized as a microvascular disease that leads to morbidity and mortality in diabetic patients.While ischemic events are commonly observed in diabetic patients,the risk for developing heart failure is also increased,independent of the severity of coronary artery disease and hypertension.This diabetes-associated clinical entity is considered a distinct disease process referred to as 'diabetic cardiomyopathy'.However,it is not clear how diabetes promotes cardiac dysfunction.Vascular endothelial dysfunction is thought to be one of the key risk factors.The impact of diabetes on the endothelium involves several alterations,including hyperglycemia,fatty acid oxidation,reduced nitric oxide (NO),oxidative stress,inflammatory activation,and altered barrier function. The current review provides an update on mechanisms that specifically target endothelial dysfunction,which may lead to diabetic cardiomyopathy. | Maura Knapp Xin Tu Rongxue Wu | 2019 | Acta Pharmacologica Sinica2019，40，1： | 34 |
| 5 | Serum vascular endothelial growth factor is a potential biomarker of metastatic recurrence after curative resection of hepatocellular carcinoma显示文摘INTRODUCTIONHepatocellular carcinoma(HCC)is one of the mostcommon malignancies in China.To date,surgery is stillthe best solution to it.However,metastatic recurrencesafter curative hepatic resections are very common.Tang etal have reported that recurrence rate within 5 years | Qi Niu Zhao You Tang Zeng Chen Ma Lun Xiu Qin Lian Hai Zhang | 2000 | World Journal of Gastroenterology2000，6，4： | 20 |
| 6 | Endothelial function and T-lymphocyte subsets in patients with overlap syndrome of chronic obstructive pulmonary disease and obstructive sleep apnea显示文摘Background:The coexistence of chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) is termed overlap syndrome (OS).COPD and OSA both have increased risks of developing cardiovascular diseases.This study aimed to explore if patients with OS exhibited a higher prevalence of cardiovascular complications,and if patients with OS exhibited vascular endothelial dysfunction and abnormalities in the cellular immune function of T lymphocytes.Methods:Totally 25 patients with stable COPD (COPD group),25 patients with OSA (OSA group),25 patients with OS (OS group),and 20 healthy adults (control group) were enrolled between January 2017 and December 2017 from the Respiratory Department of Tianjin Medical University General Hospital.The clinical characteristics of the four groups were collected and the expression levels of soluble vascular cell adhesion molecule-1 (sVCAM-1),tumor necrosis factor-α(TNF-α),and T-lymphocyte subsets were detected.One-way analysis of variance,x^2 test and Pearson correlation were used to manage the data.Results:The prevalence of hypertension and coronary heart disease was significantly higher in the OS group than in the control,OSA,and COPD groups (x^2 =20.69,P < 0.05 and x^2 =11.03,P < 0.05,respectively).The levels of sVCAM-1 and TNF-α were significantly higher in the OS group than in other groups (F =127.40,P < 0.05 and F =846.77,P < 0.05,respectively).The percentage of CD4+ lymphocytes and CD4+/CD8+ were both significantly lower in the OS group than in any other group (F =25.40,P < 0.05 and F =75.08,P < 0.05,respectively).There were significantly negative correlations in the levels of sVCAM-1 and TNF-α with CD4^+/CD8^+ lymphocytes (r =-0.77,P < 0.05 and r =-0.83,P < 0.05,respectively).Conclusions:The prevalence of hypertension and coronary heart disease was higher in patients with OS than in patients with either OSA or COPD alone.Patients with OS exhibited more severe vascular endothelial injury,stronger inflammatory response,and lower cellular immune function. | Juan Wang Xin Li Wan-Ju Hou Li-Xia Dong Jie Cao | 2019 | Chinese Medical Journal2019，，14： | 18 |
| 7 | Aspirin alleviates endothelial gap junction dysfunction through inhibition of NLRP3inflammasome activation in LPS-induced vascular injury显示文摘The loss of endothelial connective integrity and endothelial barrier dysfunction can lead to increased vascular injury, which is related to the activation of endothelial inflammasomes. There are evidences that low concentrations of aspirin can effectively prevent cardiovascular diseases. We hypothesized that low-dose aspirin could ameliorate endothelial injury by inhibiting the activation of NLRP3 inflammasomes and ultimately prevent cardiovascular diseases. Microvascular endothelial cells were stimulated by lipopolysaccharide(2 μg/mL) and administrated by 0.1–2 mmol/L aspirin. The wild type mice were stimulated with LPS(100 μg/kg/day), and 1 h later treated with aspirin(12.5, 62.5, or125 mg/kg/day) and dexamethasone(0.0182 mg/kg/day) for 7 days. Plasma and heart were harvested for measurement of ELISA and immunofluorescence analyses. We found that aspirin could inhibit NLRP3 inflammasome formation and activation in vitro in dose-dependent manner and has correlation between the NLRP3 inflammasome and the ROS/TXNIP pathway. We also found that low-concentration aspirin could inhibit the formation and activation of NLRP3 inflammasome and restore the expression of theendothelial tight junction protein zonula occludens-1/2(ZO1/2). We assume that aspirin can ameliorate the endothelial layer dysfunction by suppressing the activation of NLRP3 inflammasome. | Xing Zhou Yanjiao Wu Lifeng Ye Yunting Wang Kaimin Zhang Lingjun Wang Yi Huang Lei Wang Shaoxiang Xian Yang Zhang Yang Chen | 2019 | Acta Pharmaceutica Sinica B2019，9，4： | 13 |
| 8 | Adhesion molecule and proinflammatory cytokine gene expression in hepatic sinusoidal endothelial cells following cecal ligation and puncture显示文摘INTRODUCTIONMultiple organ dysfunction syndrome (MODS) isthought to be a frequent consequence of sepsis[1-3].Despite substantial advances in our knowledge and understanding of the basic pathophysiologic mechanisms[4-7], in critically ill patients infections and sepsis are still associated with a high mortality[8,9]. | Rong Qian Wu Ying Xin Xu Xu Hua Song Li Jun Chen Xian Jun Meng Institute of Surgical Research, General Hospital of PLA, Beijing 100853, China | 2001 | World Journal of Gastroenterology2001，7，1： | 10 |
| 9 | Relationship between vascular endothelium and periodontal disease in atherosclerotic lesions: Review article显示文摘Inflammation and endothelial dysfunction are linked to the pathogenesis of atherosclerotic disease. Recent studies suggest that periodontal infection and the ensuing increase in the levels of inflammatory markers may be associated with myocardial infarction, peripheral vascular disease and cerebrovascular disease. The present article aimed at reviewing contemporary data on the pathophysiology of vascular endothelium and its association with periodontitis in the scenario of cardiovascular disease. | Marco Aurélio Lumertz Saffi Mariana Vargas Furtado Carisi Anne Polanczyk Márlon Munhoz Montenegro Ingrid Webb Josephson Ribeiro Cassio Kampits Alex Nogueira Haas Cassiano Kuchenbecker Rosing Eneida Rejane Rabelo-Silva | 2015 | World Journal of Cardiology2015，7，1： | 9 |
| 10 | ENDOTHELIAL DYSFUNCTION IN YOUNG NORMOTENSIVE SUBJECTS WITH A FAMILY HISTORY OF ESSENTIAL HYPERTENSION显示文摘Objective To investigate whether endothelial dysfunction occurred in genetically vulnerable normotensive patients. Methods Endothelial function was assessed by high-resolution vascular ultrasound. The diameter of brachial arteries were measured at rest, during reactive hyperemia and after sublingual nitroglycerine (GTN) in 70 young subjects with a mean age of 44.7 ( 12.1 years. Among them, there were 30 patients with essential hypertension (group 1), 20 normotensive patients with a family history of hypertension (group 2) and 20 normotensive patients without a family history of cardiovascular diseases that served as controls (group 3). Results Flow-mediated dilatation of brachial arteries was significantly reduced in-group 1 and 2 when compared to group 3 (Group 1: 6.8( 3.9 vs group 2:8.0 (3.6 vs group 3:13.2 (5.9%, P<0.01). Conclusion Endothelium-dependent vasodilatation was impaired in the young normotensive patients with a family history of hypertension. | 李丽君 余卓文 耿淑仁 王志勇 李骞 段学蕴 乔义超 | 2002 | Journal of Pharmaceutical Analysis2002，14，1： | 9 |
| 11 | Alcohol-induced hypertension: Mechanism and prevention显示文摘Epidemiological, preclinical and clinical studies es-tablished the association between high alcohol con-sumption and hypertension. However the mechanism through which alcohol raises blood pressure remains elusive. Several possible mechanisms have been pro-posed such as an imbalance of the central nervous system, impairment of the baroreceptors, enhanced sympathetic activity, stimulation of the renin-angio-tensin-aldosterone system, increased cortisol levels, increased vascular reactivity due to increase in intracel-lular calcium levels, stimulation of the endothelium to release vasoconstrictors and loss of relaxation due to inflammation and oxidative injury of the endothelium leading to inhibition of endothelium-dependent nitric oxide production. Loss of relaxation due to inflamma-tion and oxidative injury of the endothelium by angio-tensin II leading to inhibition of endothelium-dependent nitric oxide production is the major contributors of the alcohol-induced hypertension. For the prevention of alcohol-induced hypertension is to reduce the amount of alcohol intake. Physical conditioning/exercise trainingis one of the most important strategies to prevent/treat chronic alcohol-induced hypertension on physiological basis. The efficacious pharmacologic treatment includes the angiotensin-converting enzyme(ACE) inhibitors or angiotensin Ⅱ type 1 receptor blockers(ARBs) which have antioxidant activity and calcium channel blockers. The most effective prevention and treatment of alcohol-induced hypertension is physical exercise and the use of ACE inhibitors or ARBs in the | Kazim Husain Rais A Ansari Leon Ferder | 2014 | World Journal of Cardiology2014，6，5： | 8 |
| 12 | Magnesium lithospermate B ameliorates microcirculation perfusion in rats by promoting vascular NO production via activating the PI3K/AKT pathway显示文摘Microcirculation morphologically refers to the blood ?ow in vessels of less than 150 μm in diameter, including arterioles, capillaries and venules, which provides nutrients and removes metabolic byproducts within tissues. Microcirculation dysfunction is involved in the pathological progress of many diseases, such as obesity, hypertension, and insulin resistance. In this study we investigated the effects of magnesium lithospermate B (MLB), an active compound of the traditional Chinese medicine Slavia miltiorrhiza, on the microcirculation dysfunction in rats and the underlying molecular mechanisms. The effects of MLB on microcirculation were assessed in vivo by measuring the hindlimb blood perfusion in dextran-induced microcirculation dysfunction rats and mesentery blood flow in anesthetized rats. We demonstrated that administration of MLB restored the impaired rat hindlimb blood ?ow and promoted the mesenteric micoperfusion in vivo. We further revealed in these two animal models that MLB treatment signi?cantly increased the production of total nitrite in vascular tissues (mesentery, aorta, and heart), which was con?rmed in human microvascular endothelial cells (HMEC-1) treated with MLB in vitro. Moreover, we showed that MLB treatment signi?cantly increased the phosphorylation of endothelium nitric oxide synthase (eNOS) via inducing AKT phosphorylation in vivo and in vitro. Co-administration of the eNOS inhibitor L-NAME (20 mg/kg) abolished the protective effects of MLB against dextran-induced microcirculation dysfunction in rats, whereas pretreatment with PI3K inhibitor LY294002 (10 μM) prevented eNOS activation in MLB-treated HMEC-1 cells. Our results suggest that MLB can restore the microcirculation dysfunction via activating eNOS, and in turn enhancing the vascular nitric oxide production, which is medicated by MLB-caused activation of the PI3K/AKT pathway. | Ying-luo Liu Xiao-yu Zhou Li-jiang Xuan | 2019 | Acta Pharmacologica Sinica2019，40，8： | 7 |
| 13 | Sphingosine-1-phosphate signaling in vasculogenesis and angiogenesis显示文摘Blood vessels either form de novo through the process of vasculogenesis or through angiogenesis that involves the sprouting and proliferation of endothelial cells in pre-existing blood vessels. A complex interactive network of signaling cascades downstream from at least three of the nine known G-protein-coupled sphingosine-1-phosphate (S1P) receptors act as a prime effector of neovascularization that occurs in embryonic development and in association with various pathologies. This review focuses on the current knowledge of the roles of S1P signaling in vasculogenesis and angiogenesis, with particular emphasis on vascular cell adhesion and motility responses. | Kelley M Argraves Brent A Wilkerson W Scott Argraves | 2010 | World Journal of Biological Chemistry2010，1，10： | 6 |
| 14 | Effect of topical 0.05% cyclosporine A on corneal endothelium in patients with dry eye disease显示文摘AIM:To determine the effect of topical 0.05%cyclosporine A(CsA) on corneal endothelium in patients with dry eye disease.·METHODS:Observational,prospective,case series study.Fifty-five eyes of 29 consecutive patients(9 males and 20 females;median age:66.8 years,interquartile range:61-73.2 years) with moderate-severe dry eye disease were evaluated.All patients were treated with topical 0.05% CsA ophthalmic emulsion twice a day in addition to lubricant eyedrops 5 times a day.The followup period was 12 months.Before treatment and at 3 and12 months post-treatment central corneal specular microscopy was performed.The endothelial cell density(ECD),coefficient of variation of cell size(CoV),and percentage of hexagonal cells(Hex %) were analyzed.·RESULTS:The median ECDs pre-treatment and at 3and 12 months post-treatment were 2 352.5/mm2(interquartile range,2 178-2548.5),2 364/mm2(interquartile range,2 174.25-2 657.5),and 2 366 cells/mm2(inter-quartile range,2 174.75-2 539.75),respectively(P =0.927,one way ANOVA).The median CoVs pre-treatment and at3 and 12 months post-treatment were 34.5(interquartile range,30-37),35(interquartile range,30-38),and 34(interquartile range,30.75-38.25),respectively(P =0.7193,one way ANOVA).The median Hex % values pre-treatment and at 3 and 12 months post-treatment were53(interquartile range,47-58),54(interquartile range,45.75-59),and 50.5(interquartile range,45.75-58),respectively(P =0.824,one way ANOVA).·CONCLUSION:Treatment of patients with dry eyedisease for 12 months with topical 0.05% CsA does not seem to cause substantial changes on corneal endothelium. | Consuelo Pérez-Rico Francisco Germain María Castro-Rebollo Agustín Moreno-Salgueiro Miguel ngel Teus | 2013 | International Journal of Ophthalmology(English edition)2013，6，4： | 6 |
| 15 | Endothelial cell metabolism in sepsis显示文摘BACKGROUND:Endothelial dysfunction in sepsis is a pathophysiological feature of septic organ failure.Endothelial cells(ECs)exhibit specific metabolic traits and release metabolites to adapt to the septic state in the blood to maintain vascular homeostasis.METHODS:Web of Science and PubMed were searched from inception to October 1,2022.The search was limited to the English language only.Two reviewers independently identified studies related to EC metabolism in sepsis.The exclusion criteria were duplicate articles according to multiple search criteria.RESULTS:Sixty articles were included,and most of them were cell and animal studies.These studies reported the role of glycolysis,oxidative phosphorylation,fatty acid metabolism,and amino acid metabolism in EC homeostasis.including glycolysis,oxidative phosphorylation,fatty acid metabolism and amino acid metabolism.However,dysregulation of EC metabolism can contribute to sepsis progression.CONCLUSION:There are few clinical studies on EC metabolism in sepsis.Related research mainly focuses on basic research,but some scientific problems have also been clarified.Therefore,this review may provide an overall comprehension and novel aspects of EC metabolism in sepsis. | Jue-xian Wei Hui-lin Jiang Xiao-hui Chen | 2023 | World Journal of Emergency Medicine2023，14，1： | 5 |
| 16 | Role of oxidative stress in endothelial insulin resistance显示文摘The International Diabetes Federation estimates that 316million people are currently affected by impaired glucose tolerance(IGT).Most importantly,recent forecasts anticipate a dramatic IGT increase with more that 470million people affected by the year 2035.Impaired insulin sensitivity is major feature of obesity and diabetes and is strongly linked with adverse cardiometabolic phenotypes.However,the etiologic pathway linking impaired glucose tolerance and cardiovascular disease remains to be deciphered.Although insulin resistance has been attributed to inflammatory programs starting in adipose tissue,emerging evidence indicates that endothelial dysfunction may represent the upstream event preceding peripheral impairment of insulin sensitivity.Indeed,suppression of reactive oxygen species-dependent pathways in the endothelium has shown to restore insulin delivery to peripheral organs by preserving nitric oxide(NO)availability.Here we describe emerging theories concerning endothelial insulin resistance,with particular emphasis on the role oxidative stress.Complex molecular circuits including endothelial nitric oxide synthase,prostacyclin synthase,mitochondrial adaptor p66^(Shc),nicotinamide adenine dinucleotide phosphate-oxidase oxidase and nuclear factor kappa-B are discussed.Moreover,the review provides insights on the effectiveness of available compounds(i.e.,ruboxistaurin,sildenafil,endothelin receptor antagonists,NO donors)in restoring endothelial insulin signalling.Taken together,these aspects may significantly contribute to design novel therapeutic approaches to restore glucose homeostasis in patients with obesity and diabetes. | Francesco Paneni Sarah Costantino Francesco Cosentino | 2015 | World Journal of Diabetes2015，6，2： | 5 |
| 17 | Outgrowth endothelial cells form a functional cerebral barrier and restore its integrity after damage显示文摘Breakdown of blood-brain barrier,formed mainly by brain microvascular endothelial cells(BMECs),represents the major cause of mortality during early phases of ischemic strokes.Hence,discovery of novel agents that can effectively replace dead or dying endothelial cells to restore blood-brain barrier integrity is of paramount importance in stroke medicine.Although endothelial progenitor cells(EPCs)represent one such agents,their rarity in peripheral blood severely limits their adequate isolation and therapeutic use for acute ischemic stroke which necessitate their ex vivo expansion and generate early EPCs and outgrowth endothelial cells(OECs)as a result.Functional analyses of these cells,in the present study,demonstrated that only OECs endocytosed DiI-labelled acetylated low-density lipoprotein and formed tubules on matrigel,prominent endothelial cell and angiogenesis markers,respectively.Further analyses by flow cytometry demonstrated that OECs expressed specific markers for sternness(CD34),immaturity(CD133)and endothelial cells(CD31)but not for hematopoietic cells(CD45).Like BMECs,OECs established an equally tight in vitro model of human BBB with astrocytes and pericytes,suggesting their capacity to form tight junctions.Ischemic injury mimicked by concurrent deprivation of oxygen and glucose(4 hours)or deprivation of oxygen and glucose followed by reperfusion(20 hours)affected both barrier integrity and function in a similar fashion as evidenced by decreases in transendothelial electrical resistance and increases in paracellular flux,respectively.Wound scratch assays comparing the vasculoreparative capacity of cells revealed that,compared to BMECs,OECs possessed a greater proliferative and directional migratory capacity.In a triple culture model of BBB established with astrocytes,pericytes and BMEC,exogenous addition of OECs effectively repaired the damage induced on endothelial layer in serum-free conditions.Taken together,these data demonstrate that OECs may effectively home to the site of vascular injury and repair the damage to maintain(neuro)vascular homeostasis during or after a cerebral ischemic injury. | Rais Reskiawan Abdulkadir Mansour Alwjwaj Othman Ahmad Othman Kamini Rakkar Ulvi Bayraktutan | 2020 | Neural Regeneration Research2020，15，6： | 5 |
| 18 | mTORC2 facilitates endothelial cell senescence by suppressing Nrf2 expression via the Akt/GSK-3β/C/EBPα signaling pathway显示文摘Vascular endothelial cell senescence is a leading cause of age-associated and vascular diseases. Mammalian target of rapamycin complex 2 (mTORC2) is a conserved serine/threonine (Ser/Thr) protein kinase that plays an important regulatory role in various cellular processes. However, its impact on endothelial senescence remains controversial. In this study we investigated the role and molecular mechanisms of mTORC2 in endothelial senescence. A replicative senescence model and H2O2-induced premature senescence model were established in primary cultured human umbilical vein endothelial cells (HUVECs). In these senescence models, the formation and activation of mTORC2 were significantly increased, evidenced by the increases in binding of Rictor (the essential component of mTORC2) to mTOR, phosphorylation of mTOR at Ser2481 and phosphorylation of Akt (the effector of mTORC2) at Ser473. Knockdown of Rictor or treatment with the Akt inhibitor MK-2206 attenuated senescence-associated β-galactosidase (β-gal) staining and expression of p53 and p21 proteins in the senescent endothelial cells, suggesting that mTORC2/Akt facilitates endothelial senescence. The effect of mTORC2/Akt on endothelial senescence was due to suppression of nuclear factor erythroid 2-related factor 2 (Nrf2) at the transcriptional level, since knockdown of Rictor reversed the reduction of Nrf2 mRNA expression in endothelial senescence. Furthermore, mTORC2 suppressed the expression of Nrf2 via the Akt/GSK-3β/C/EBPα signaling pathway. These results suggest that the mTORC2/Akt/GSK-3β/C/EBPα/Nrf2 signaling pathway is involved in both replicative and inducible endothelial senescence. The deleterious role of mTORC2 in endothelial cell senescence suggests therapeutic strategies (targeting mTORC2) for aging-associated diseases and vascular diseases. | Han-wei Yang Hui-ling Hong Wen-wei Luo Chun-mei Dai Xin-yi Chen Lu-ping Wang Qian Li Zi-qing Li Pei-qing Liu Zhuo-ming Li | 2018 | Acta Pharmacologica Sinica2018，39，12： | 3 |
| 19 | Chinese herbal remedies affecting thrombosis and hemostasis: A review显示文摘Acute coronary syndrome, stroke and other ischemic events continue to be the most common causes of mortality and morbidity in the world, and their incidence is rapidly increasing in the developing nations. These cardiovascular disorders clinically manifest as acute atherothrombotic events. Application of oral antiplatelet drugs is a milestone in the therapy of cardiovascular diseases. However, the limited efficacy of these drugs in the setting of arterial thrombosis, their unfavorable side effects, cost-to-benefit issues and the drug resistance phenomenon substantiate the need for the development of new and more efficacious antithrombotic drugs. In recent years, with the progress in the study of the Chinese medicine pharmacology, many Chinese herbs and formulas, as well as active constituents have been reported to possess not only effects on platelet aggregation and activation but also beneficial roles in vascular functions. Compared with currently used antithrombotic agents, herb remedies exert antithrombotic effects in a multi-pathway and multi-target manner. This paper will cover the progress in research on the ameliorating effects of herbal remedies on thrombosis, with focusing on their protection of vascular endothelial cells and inhibition of platelet activation. | Quan Li Jing-Yu Fan Jing-Yan Han | 2015 | World Journal of Traditional Chinese Medicine2015，1，2： | 3 |
| 20 | Morphometric study of endothelial wound-healing following penetrating keratoplasty显示文摘Twenty samples of endothelia removed from normal and post penetrating keratoplas-ty (0.5,1,2,3 months after penetrating keratoplasty) were observed by scanning electron mi-croscopy.The photographs of the endothelia in graft-host junction were analyzed by computer-assisted image analysis system,and the morphometric indexes examined were area of the cells,perimeters,density,figure coefficient,long axis,coefficient of variation of the area,and oth-ers.Results showed that the morphology and the density of the endothelial cells changed obvi-ously after operation and improved slowly but progressively with time although at 3 monthspostoperatively some differences still existed.By using the new techniques,the experiment con-firmed and enriched the theories on the corneal endothelial wound-healing,revealing some ofthe new characters of the endothelial wound-healing following penetrating keratoplasty. | 蒋华 宋振英 林庆华 | 1993 | Journal of Medical Colleges of PLA(China)1993，8，3： | 3 |
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