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Journal of Pharmaceutical Analysis 2003年第2期15卷 196-198,201页

作者：林蓉刘俊田甘伟杰 Dept. of Pharmacology Medical School of Xi ’an Jiaotong University

Objective To study the effects of different concentrations of Quercetin on nitric oxide (NO) production and membrane fluidity of the injured human umbilical vein vascular endothelial cell line(ECV 304) with hypoxia and the lack of glucose. Methods The experiments were performed in the culture of ECV 304 injured with hypoxia and the lack of glucose in vitro. The releases of intracellular lactate dehydrogenase(LDH) of ECV 304 was measured with automatic biochemistry analysis. NO level of ECV 304 was monitored with colorimetry. The membrane fluidity of ECV 304 was measured with the fluorescence polarization method. Results After ECV 304 was cultured in hypoxia and the the lack of glucose for 24 hours, the release of LDH and the membrane fluidity were increased significantly; NO level was decreased. Preincubation of ECV 304 with 20, 80,160 μ mol·L -1  of Quercetin for 24 hours reduced LDH activity, membrane fluidity and increased the level of NO in hypoxia and the lack of glucose induced ECV 304. Conclusion These results demonstrate that Quercetin can produce the protective effect on hypoxia and the lack of glucose induced injury of ECV 304 by increasing release of NO and changing membrane fluidity.

关键词： quercetin(Que) Endothelial cells membrane fluidity hypoxia and the lack of glucose

Matrix Stiffness-Induced Transcriptome Alterations and Regulatory Mechanisms Revealed by RNA-Seq in Endothelial cells

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Journal of Biomaterials and Nanobiotechnology 2022年第3期13卷 61-79页

作者： Chao Zhang Xiaomei Han Jin Xu Yue Zhou School of Biomedical Engineering Shanghai Jiao Tong University Shanghai China

Changes in vascular stiffness are associated with the development and progression of many diseases, especially in cardiovascular disease. However, the effect of vascular stiffness on the Endothelial cells (ECs) is not fully understood. Therefore, this study aims to determine the gene expression changes of ECs cultured on the matrices with different stiffness (1 kPa and 40 kPa, respectively) by RNA-seq, thereby broadening the knowledge between mechanics and biology. We obtained 1775 differentially expressed genes (DEGs) by RNA-seq, with 450 up-regulated and 1325 down-regulated DEGs in ECs cultured on soft matrix (1 kPa) compared to those cultured on stiff matrix (40 kPa). After that, we performed a series of functional enrichment analyses based on DEGs and found that DEGs were enriched in many signaling pathways like adhesion junction. Furthermore, transcription factor (TF) target gene prediction analysis and protein-protein interaction (PPI) analysis were also conducted. We found that mechanotransduction signaling related TFs such as BRD4 are involved in. And in the PPI analysis, some genes encoding extracellular matrix proteins such as fibronectin 1 (FN1) were identified as the hub genes. In order to confirm the RNA-seq results, we performed real-time qPCR analysis on the genes of interest, including FN1, collagen α2 (IV) chain, matrix metalloproteinase-14 and integrin α5, and found that the expression levels of all these genes were down-regulated on soft matrix, suggesting that soft matrix caused by pathological conditions may directly attenuate vascular barrier function. This study offers the insights about the effects of physical stimulation on cells, paving a way for vascular tissue engineering, regenerative medicine, disease modeling and therapies.

关键词： Endothelial cells Matrix Stiffness RNA-Seq Cell-Cell Junctions Extracellular Matrix

The protective effect of Ligustrazin on the Bid and Caspase-3,8,9 of Endothelial cells

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The protective effect of Ligustrazin on the Bid and Caspase-...

中国食品科学技术学会第八届年会暨第六届东西方食品业高层...

作者： Xian-feng Zhong Ting Luo Ze-yuan Deng~* (State Key Laboratory of Food Science and Technology,Nanchang University,Nanchang 330047,China)

＜正＞Objective:The present study was designed to test the hypothesis that Ligustrazin can inhibit hydrogen peroxide（H2O2）-induced injury in human umbilical vein Endothelial cells（HUVECs）,and Ligustrazin has a preventive effect on atherosclerosis at the genetic level.Methods:The oxidative injury model was established with H2O2.HUVECs were treated with different concentrations of Ligustrazin in the presence of H2O2.The protective effects of Ligustrazin against H2O2-injury were investigated in the present study.Results:HUVECs incubated with 200?mol/L H2O2 had significantly decreased in cell viability,which was accompanied with apparent cells apoptosis and the up-regulative expression level of Bid,Caspase-3,8,9 mRNA.In addition,the results of quantitative real-time polymerase chain reaction （qRT-PCR）indicated that pretreatment with Ligustrazine down-regulated the expression of Bid and Caspase-3,8,9 mRNA,which had a key role in H2O2-induced cell apoptosis.Conclusion:The study shows that Ligustrazine can protect Endothelial cells against oxidative injury induced by H2O2,suggesting that Ligustrazine is a potential compound for the prevention and treatment of atherosclerosis.

关键词： Ligustrazine oxidative damage Endothelial cells protective effects qRT-PCR

Inhibitory effect of rosiglitazone on C-reactive protein production induced by angiotensin Ⅱ in human aortic Endothelial cells via ROS and mitogen activated protein kinases signaling

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Inhibitory effect of rosiglitazone on C-reactive protein pro...

中国药理学会第十一次全国学术会议

作者： HAN Chun-jie~1,LIU Jun-tian~2,CUI Mu~(2,3),LI Ming~2,PENG Xiao-ming~2,MAO Jun-jun~2 (1.Department of Pharmacology,Shannxi Institute For Food And Drug Control,Xi’an 710061,China 2.Department of Pharmacology,Xi’an Jiaotong University School of Medicine,Xi’an 710061,’ China 3.Nursing Department,Xi’an Medical University,Xi’an 710021,China)

OBJECTIVE To observe the effects of rosiglitazone on signaling pathway of angiotensinⅡ(AngⅡ) -induced C-reactive protein(CRP) expression in human aortic Endothelial cells(HAECs).METHODS HAECs were pretreated with the different concentrations of rosiglitazone 18 h before stimulation with Ang II for 12 h.Then,mRNA of CRP and AT,was analyzed by RT-PCR, and the protein expressions of CRP,ATI,p-JNK,p-ERK1/2,JNK and ERK1/2 in HAECs were analyzed by western blot respectively. HAECs were pretreated with losartan,PD123319 for 1 h or rosiglitazone for 18 h prior to stimulation with AngⅡfor 12 h.Then, the cells were incubated for 1 h with H2DCF-DA.Finally,the fluorescent intensity was measured by a fluorescence microscope.RE- SULTS Pretreatment of the cells with rosiglitazone for 18 h obviously reduced AngⅡ-induced mRNA and protein expressions of CRP and AT.Losartan and rosiglitazone obviously inhibited AngⅡ-stimulated ROS generation,while PD123319 showed no significantly inhibitory effect on ROS production in HAECs.Preincubation of the cells with rosiglitazone for 18 h obviously downregulated AngⅡ-caused phosphorylation of ERK1/2 and JNK in HAECs.Thus,rosiglitazone is able to inhibit AngⅡ-induced CRP expression in HAECs,and probably through interfering with AT-ROS-MAPK signal pathway.DISCUSSION As an inflammatory molecule,CRP plays a direct role in atherogenesis.Our previous study confirmed that AngⅡis capable of inducing CRP generation in HAECs,which is through AT-ROS-ERK1/2 and JNK-NF-κB signaling pathway.In the present study,we observed that rosiglitazone attenuated AngⅡ-induced CRP expression in HAECs,which implies that rosiglitazone may counteract vascular inflammation and thus exerts a beneficial effect in prevention of atherosclerosis.It is well known that most of the deleterious effects of AngⅡare accomplished through AT receptor.The present results showed that AngⅡupregulates AT expression,whereas rosiglitazone reduced AngⅡ-induced AT expression in HAECs.As AT receptor mediates AngⅡ-induced CRP expression in HAECs

关键词： rosiglitazone angiotensinⅡ C-reactive protein Endothelial cells

Advanced Glycation End Products Upregulates The Expression Of Connexin 43 Via ERK MAPK And PI3K/Akt Pathways In Human Endothelial cells

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Advanced Glycation End Products Upregulates The Expression O...

第五届钱江国际心血管病会议暨2011浙江省心血管病年会

作者： Yanbo Zhao Shengjie Xu Chongying Jin Guosheng Fu Shaoxiang Weng

＜正＞Intercellular communication through gap junctions plays an essential role in maintaining the functional integrity of vascular endothelium.Despite emerging evidence suggests that advanced glycation end products（AGEs） may impair endothelial function.However,its effect on connexin43 （Cx43） gap junction in Endothelial cells remains unexplored.Here we investigated the effect Of AGEbovine serum albumin（AGE-BSA） on Cx43 gap junction in Endothelial cells.The levels of Cx43 protein in human umbilical vein Endothelial cells（HUVECs） was significantly increased by AGE-BSA treatment, accompanied by RAGE overexpression.This augmentation can be reversed by RAGE knockdown.In addition,AGE-BSA activated ERK,P38,and JNK mitogen-activated protein kinases（MAPKs）,which were supposed to participate in the regulation of Cx43.A MEK inhibitor PD98059,but not SB203580（a p38 kinase inhibitor） or SP600125（a JNK kinase inhibitor）,abolished the effects of AGE-BSA on Cx43 expression.Moreover,both Akt and PKC phosphorylation were time-dependently augmented by AGEBSA, PI3K inhibitor LY294002（but not GF109203X,a PKC inhibitor） blocked the effects of AGE-BSA on Cx43 gap junctions.Taken together,AGE-BSA upregulated Cx43 expression via AGE-RAGE signaling, ERK MAPK and PI3K/Akt Signal transduction pathways appear to be involved in these processes.

关键词： advanced glycation end products Endothelial cells connexin43 gap junction

Effects of Angiotensin Ⅱ and Valsartan on the Expression of ATR_1/ATR_2 Receptors,eNOS in Vascular Endothelial cells

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South China Journal of Cardiology 2008年第4期9卷 188-192,208页

作者：王炎汪培华汪道文 Cardiovascular Institute First Affiliated Hospital of Guangxi Medical University The Institute of Hypertension and Department of Internal Medicine Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology

Background Angiotensin Ⅱ type 1 receptor (ATR1) / Angiotensin Ⅱ type 2 receptor (ATR2) usually interact with each other in their expression and physiological functions, and nitric oxide (NO) is always involved in ATR1 / ATR2 regulation in vivo. Endothelial cells play a crucial role in the maintenance of vascular function and in the prevention of cardiovascular diseases. Objectives To investigate the effects of angiotensin Ⅱ (Ang Ⅱ) and ATR1 blocker valsartan on ATR1, ATR2 expression and their relation with endothelial nitric oxide synthase (eNOS) expression, and NO production in cultured vascular Endothelial cells. Methods Human umbilical vein endothelial cell line (HUVEC) and bovine aortic endothelial cell (BAEC) were used. BAEC were isolated from aorta of newborn calf by enzyme digestion and cells of 3-5 passages were used. cells were incubated with vehicle, Ang Ⅱ, valsartan, or Ang Ⅱ plus valsartan respectively for various periods. ATR1, ATR2, eNOS expression and NO production were detected. Results Incubation with AngⅡ or valsartan apparently downregulated ATR1 mRNA and protein expression in vascular Endothelial cells, and the combination effect of the two drugs were more apparent. Ang Ⅱ showed a transient slightly promotive effect on eNOS and NO generation in BAEC and an apparently inhibitory effect with prolonged incubation, while valsartan can apparently reverse those effects. Conclusions Both Ang Ⅱ and valsartan downregulated the expression of ATR1 in vascular Endothelial cells. The synergistic effect of the two drugs was more apparent. Prolonged incubation with Ang Ⅱ can apparently inhibit eNOS expression and NO production in Endothelial cells, while valsartan can apparently reverse that inhibitory effect.

关键词： angiotensin Ⅱ Endothelial cells valsartan

Lymphocytes favor the attachment of CD11A-targeted microbubbles with Endothelial cells in vitro

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Lymphocytes favor the attachment of CD11A-targeted microbubb...

2011年全国压电和声波理论及器件应用研讨会

作者： Wei YANG~1 Fei YAN~1 Juan-Juan CHEN~2 Hai-Rong ZHENG~(1,3,*) 1 Shenzhen Institutes of Advanced Technology,Chinese Academy of Sciences,Shenzhen 518055 2 Molecular Medicine and Cancer Research Center,Chongqing Medical University,Chongqing 400016 3 Key Lab of Health Informatics of Chinese Academy of Sciences,Shenzhen 518055

＜正＞Ultrasound molecular imaging may provide new insights into the early detection and diagnose of diseases,such as atherosclerosis,thrombosis as well as inflammations by the attachment of various targeted contrast agents with disordered endothelium.However,molecular imaging of disordered endothelium in large and middle-sized arteries

关键词： Targeted microbubbles Lymphocyte Endothelial cells Adhesion

The crosstalk between nitrosative stress and cellular autophagy-lysosome process in Endothelial cells during brain ischemia

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The crosstalk between nitrosative stress and cellular autoph...

中国药理学会第十一次全国学术会议

作者： TAO Rong-rong,HUANG Ji-yun,ZHANG Geng-sheng,LIAO Mei-hua,HAN Feng (Institute of Pharmacology,Toxicology and Biochemical Pharmaceutics,Zhejiang University,Hangzhou,China)

OBJECTIVE The present study was desighed to determine the causative links and precise correlations among nitro-sative stress,the cellular autophagy-lysosome process,and neurovascular damage during cerebral ischemia.METHODS To mimic ischemic-like conditions in vitro,endothelial cell cultures were exposed to permanent glucose deprivation and hypoxia for 2,6,12 and 24 h.The male rats were subjected to general anesthesia,after which 1000 non-radioactive microspheres were injected into the left carotid artery.The ipsilateral hemisphere was dissected out for morphological and biochemical analysis.RESULTS In parallelled with OGD-induced peroxynitrite formation,a rapid induction of microtubule-associated protein 1 light chain 3(LC3) -Ⅰ/Ⅱconversion and green fluorescent protein-LC3 punctae accumulation were observed in Endothelial cells.The Western blot analyses indicated that OGD induced elevations in Lamp2 and cathepsin B protein levels.Furthermore,cultured Endothelial cells treated with peroxynitrite(1-50μmol·L) exhibited a concentration-dependent change in the pattern of autophagy-lysosome signaling.Intriguingly,OGD-induced autophagy -lysosome processes were attenuated by PEP-19 overexpression and by a small-interfering RNA(siRNA)-mediated knockdown of eNOS.The current study also focused on the morphological and biochemical aspects of autophagy-lysosome process at miceovessels during the pathological process of cerebral microemboli in vivo.The importance of nitrosative stress in ischemia-induced autophagy-lysosome cascades is further supported by our finding that pharmacological inhibition of nitrosative stress by melatonin partially inhibits the ischemia-induced autophagy-lysosome cascade and the degradation of the tight junction proteins.CONCLUSION Based on our observations, we predict that peroxynitrite-mediated nitrosative stress at least partially potentiates autophagy-lysosome signaling during sustained ischemic insult-induced endothelial cell damage.

关键词： nitrosative stress brain ischemia Endothelial cells autophagy tight junction

A natural squamosamide derivative FLZ inhibits homocysteine-induced rat brain microvascular Endothelial cells dysfunction

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A natural squamosamide derivative FLZ inhibits homocysteine-...

中国药理学会第十一次全国学术会议

作者： KANG Rui-xia,ZHANG Jian-jun (Key Laboratory of Bioactive Substances and Function of Natural Medicine,Institute of Material Medica, CAMS&PUMC,Beijing 100050,China)

OBJECTIVE Compound FLZ is a novel synthetic squamosamide cyclic analogue with several phenolichydroxy groups.Previous researches have demonstrated that FLZ exhibits strong anti-oxidative and neuroprotective activities in AD and PD models. Hyperhomocysteinemia(HHcy) is believed to induce endothelial dysfunction,which is an independent risk factor for atherosclerosis and vascular diseases.This study was designed to examine whether FLZ has protective effect against HHcy-induced primary cultured rat brain microvascular Endothelial cells(rBMEC) injury.METHODS Cell survival was measured by MTT assay.Cell nuclei were observed by Hochest 33342 staining.Senescent cells were detected by senescence associatedβ-galactosidase(SA-β-gal) staining. ROS was measured by DCF fluorescent microscopy.The NO production and NOS activity were measured by biochemical methods.HHcy -induced expression of NF-κB,p53,Noxa and Fas,the release of mitochondrial cytochrome c were measured by Western blot analysis. RESULTS In this study,we found that FLZ(0.1-10μmol·L) may antagonize homocysteine(1 mmol·L) induced cell death(88%when FLZ was 10μmol·L vs.55%for Hcy,Pcells increase,which were correlated with the decrease of ROS accumulation,NO production and NOS activity.Western blotting analyses showed FLZ could inhibit the activation of NF-κB,upregulation of p53,Noxa and Fas.Pretreatment of FLZ also blocked mitochondrial cytochrome c release.CON- CLUSION These findings suggest that FLZ has protective action against HHcy-induced toxicity in rBMECs,which may have implications FLZ may have therapeutic potential for the prevention of cardiovascular diseases.

关键词： FLZ homocysteine Endothelial cells ROS FAS p53

Involvement of BMP Signaling in Proliferation of Human Coronary Artery Endothelial cells

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South China Journal of Cardiology 2008年第2期9卷 81-87页

作者：郭素珍 Terence M Doherty 徐军 Andres J.Espinoza The Atherosclerosis Research Center Division of Cardiology Department of Medicineand The Burns and Allen Research Institute Cedars-Sinai Medical Centerand David Geffen School of Medicine at UCLA Los Angeles

Objectives To test the hypotheses that bone morphogenetic protein（BMP） signaling pathway components are expressed in arterial Endothelial cells （ECs） and that BMP signaling influences endothelial cell（EC） proliferation. Methods We used cell culture and RT-PCR to determined mRNA expression of BMP receptors （BMPR）-IA, -IB, and II, Smads 1,4, 5, 6, and 7, and in cultured human coronary artery ECs at baseline and after stimulation with BMP2 （300 ng/mL for 6 hr）, non-radioactive cell proliferation to examine cell proliferation. Results Proteasome inhibition has been previously shown to enhance BMP signaling by preventing degradation of BMP pathway components. Therefore, identical experiments were also performed in the presence of the proteasome inhibitor epoxomicin. ECs expressed mRNA for BMPRs IA and II, Smads 1,4, 5, 6, 7, and stimulation with either BMP2 or epoxomicin resulted in a significant increase in EC proliferation measured after 48 hours in a dose-dependent fashion. Proliferation was accompanied by a marked increase in proliferating cell nuclear antigen （PCNA） expression. Toxicity was observed at high doses of epoxomicin. Conclusions All major BMP signaling molecules are expressed by vascular ECs and expression of these are affected by both BMP2 and epoxomicin. BMP2 may regulate EC proliferation, suggesting a possible role in vascular homeostasis and vascular pathologies involving EC denudation or proliferation.

关键词： bone morphogenetic proteins bone morphogenetic protein receptors Endothelial cells