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Open Journal of Pediatrics 2016年第4期6卷 324-332页

作者： Qidi Peng Liping Yuan Yan Bo Xiaoyan Guo Hu Bo Department of Pediatrics First Affiliated Hospital of Anhui Medical University Hefei China Department of Medical Technology Anhui Medical College Hefei China

Acidosis in local environment plays a critical role in cell injury. One key mediator of acidosis-induced cell injury is the acid-sensing ion channels (ASICs), particularly ASIC1a. Herein, we investigated the role of ASIC1a in acid-induced vascular endothelial cell injury of Henoch-Schonlein purpura (HSP) children. Acid-induced ASIC1a, Calpain and Calcineurin expression in vascular endothelial cells pretreated with IgA1 isolated from HSP were detected by real time quantitative polymerase chain reaction and western blot methods, respectively. cell cytotoxicity was measured by interleukin-8 and nitric oxide production with ELISA. The results showed acid-induced ASIC1a, Calpain and Calcineurin expression in cells increased, especially at PH6.5. The cytotoxicity of vascular endothelial cells was increased by extracellular acidosis. Moreover non-specific or specific blockers of ASIC1a, Amiloride and PcTX-1 could remarkably decrease these parameters. These findings show that increased [Ca2+]i, mediated via ASIC1a, might contribute to acid-induced vascular endothelial cell injury of HSP.

关键词： Acid-Sensing Ion Channels (ASICs) vascular endothelial cell Henoch-Schönlein Purpura (HSP)

A New Rat Model of Cerebral Infarction Based on the Injury of vascular endothelial cell

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Chinese Journal of Integrated Traditional and Western Medicine 2005年第3期11卷 195-200页

作者：陈懿葛金文邓冰湘 Department of Physiology Hunan University of Traditional Chinese Medicine Department of Science and Technology Hunan University of Traditional Chinese Medicine

Objective： A new rat model of cerebral infarction was developed to elucidate the contribution of vascular endothelial cell during focal cerebral infarction formation. Methods： Forty-eight Sprague-Dawley （SD） rats were randomly divided into the model group, sham operation group, and control group for indexes observation of triphenyltetrazolium chloride （TTC） dyeing, neurological deficit, plasma tissue-type plasminogen activator （tPA） activity, plasminogen activator inhibitor （PAl） activity, thromboxane B2（TXB2） content, and 6-keto-prostaglandin （6-keto-PGF1α） content. Results：（1） The highest neurological score appeared at 6 h after operation, descending significantly at sequential time. （2） Using TTC dyeing and optical microscope technique, pathological changes in brains were observed. （3） Compared with control group and sham operation groups, there was a decrease in tPA activity of model rats at the initial 12 h after injection of sodium laurate （P〈0.05）, PAl activity decreased markedly in the model group at 24 h after injection of sodium laurate. （4） In plasma TXB2 concentration reached the highest level compared at 6 h after injection of sodium laurate, but there were not obvious differences in plasma 6-keto-PGF1α concentration among all groups （P〉 0.05）. Conclusion. Focal cerebral infarction in rats could be induced by some sodium laurate, showing ischemic cerebrum necrosis, function disorder of vascular endothelium-platelet, fibrinolysis abnormality. This model could play an important role in researching the contribution of vascular endothelial cell during cerebral infarction development, preventing and curing by traditional Chinese medicine.

关键词： sodium laurate cerebral infarction vascular endothelial cell

A New Rat Model of Cerebral Infarction Based on the Injury of vascular endothelial cell

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A New Rat Model of Cerebral Infarction Based on the Injury o...

Construction of human VEGF165 gene eukaryotic expression plasmid and its effect on proliferation of vascular endothelial cells

湖南省生理科学学会2004年度学术年会

作者：陈懿葛金文邓冰湘 Department of Physiology Hunan University of Traditional Chinese Medicine Changsha410007China Lab of vascular Biology Hunan University of Traditional Chinese MedicineChangsha410007China Department of Physiology Hunan University of Traditional Chinese MedicineChangsha410007China

＜正＞Objective A new rat model of cerebral infarction was developed to elucidate the contribution of vascular endothelial cell during focal cerebral cerebral infarction formation. Methods Forty-eight Sprague-Dawley（SD） rats were randomly divided into the model group with 21 rats in which sodium laurate was injected into the left internal carotid artery, sham operation group with 21 rats in which sodium laurate was substituted with 0.9% sodium chloride solution, and control group with 6 rats without any treatment. 7 rats were respectively executed for indexes observation in model group and sham operation group at 6, 12, 24 h after operation, as well as 6 rats in control group. These indexes included triphenyltetrazolium chloride （TTC） dyeing, neurological deficit, plasma tissue-type plasminogen activator（tPA） activity, plasminogen activator inhibitor（PAI） activity, thromboxaneB2 （TXB2） content, and 6-keto-PGF1 α content.

关键词： sodium laurate cerebral infarct vascular endothelial cell

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Hepatobiliary & Pancreatic Diseases International 2005年第3期4卷 364-369页

作者： Organ Grafting Center, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003 , China Department of Cardiothoracic Surgery, the General Hospital of Daqing Oil Field, Daqing 163001 , China and Department of vascular Surgery, First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China Organ Grafting Center First Affiliated Hospital Zhejiang University School of Medicine Hangzhou 310003 China.

After organ transplantation, rapid repair of injured vascular endothelial cell (VEC) is a key to prevent graft chronic dysfunction besides control of immunological rejection. Many studies have confirmed that vascular endothelial growth factor 165 (VEGF165) could accelerate the repair of VEC injury, decrease thrombosis and thrombotic occlusion, and inhibit hyperplasia of the intima. This study was designed to construct eukaryotic expression plasmid pBudCE4.1/VEGF165, and observe its effect on the prolife ration of VEC. METHODS:The VEGF165 gene cloned from human heart tissue by RT-PCR was cloned into eukaryotic expression plasmid pBudCE4.1. The recombinant expression plasmid pBudCE4.1/VEGF165 was identified by restriction enzyme (Hind III and BamH I) digestion analysis, and was sequenced. The pBudCE4.1/VEGF165 was introduced into VEC through lipofection transfection. The VEGF165 mRNA expression by Northern blot and VEGF165 protein expression was detected by immunocytochemical staining. The effect of expression protein on VEC proliferation was detected by flow cytometry. RESULTS:The RT-PCR product of the VEGF165 gene was about 576bp. Sequencing analysis revealed that the sequence of the amplified VEGF165 gene was identical with that in GenBank. Restrictive enzyme digestion analysis showed that recombinant expression plasmid pBudCE4.1/ tVEGF165 had been constructed successfully. The expression of VEGF165 at mRNA and protein levels in the transformed VSMCs had been demonstrated by Northern blot and immunocytochemical staining respectively. The expressed product of VEGF165 could notably accelerate the proliferation of VECs. CONCLUSIONS:pBudCE4.1/VEGF165 is successfully cons- tructed and is expressed in VECs. Expressed VEGF165 can accelerate the VEC proliferation. The present study has laid a foundation for potential use of VEGF165 gene transfection to prevent and treat vascular stenosis in the transplanted organ.

关键词： eukaryotic expression plasmid vascular endothelial grow factor 165 vascular endothelial cell gene transfer organ transplantation

Identification of Peptides Inhibiting Adhesion of Monocytes to the Injured vascular endothelial cells through Phage-displaying Screening

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Acta Biochimica et Biophysica Sinica 2005年第4期37卷 227-233页

作者： Yu GUO~1 Jia ZHANG~2 Ji-Cheng WANG~2 Feng-Xiang YAN~1 Bing-Yang ZHU~1 Hong-Lin HUANG~1 Duan-Fang LIAO~(1,2) ~1Institute of Pharmacy and Pharmacology,and ~2Institute of Single Nucleotide Polymorphism,Nanhua University,Hengyang 421001,China InstituteofPharmacyandPharmacology NanhuaUniversityHengyang421001China

Using oxidized low-density lipoprotein (LDL)-injured vascular endothelial cells (ECs) as targetcells,peptides specifically binding to the injured ECs were screened from a phage-displaying peptide libraryby using the whole-cell screening technique after three cycles of the“adsorption-elution-amplification”*** phage clones were identified by ELISA,and the inserted amino acid sequences in thedisplaying peptides were deduced from confirmation with DNA *** adhesion rate of ECs tomonocytes was evaluated by cell *** activity of endothelial nitric oxide synthase (eNOS),and theexpression levels of caveolin-1 and intercellular adhesion molecule-1(ICAM-1)were determined by *** positive clones specifically binding to injured ECV304 endothelial cells were selected fromfourteen ***,four phages had peptides with tandem leucine,and two of these even sharedan identical *** analysis demonstrated that the YCPRYVRRKLENELLVL peptide shared bytwo clones inhibited the expression of ICAM-1,increased nitric oxide concentration in the culture media,andupregulated the expression of caveolin-1 and *** a result,the adhesion rate of monocytes to ECV304cells was significantly reduced by 12.1%.These data suggest that the anti-adhesion effect of these novelpeptides is related to the regulation of the caveolin-1/nitric oxide signal transduction pathway,and could be ofuse in potential therapeutic agents against certain cardiovascular diseases initiated by vascular endothelial celldamage.

关键词： random peptide phage library vascular endothelial cell whole-cell screening cell adhesion caveolin-1 eNOS

Generation of rat blood vasculature and hematopoietic cells in rat-mouse chimeras by blastocyst complementation

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Journal of Genetics and Genomics 2020年第5期47卷 249-261页

作者： Xiaomin Wang Hui Shi Juanjuan Zhou Qingjian Zou Quanjun Zhang Shixue Gou Pengfei Chen Lisha Mou Nana Fan Yangyang Suo Zhen Ouyang Chengdan Lai Quanmei Yan Liangxue Lai CAS Key Laboratory of Regenerative Biology Guangdong Provincial Key Laboratory of Stem Cell and Regenerative MedicineSouth China Institute for Stem Cell Biology and Regenerative MedicineGuangzhou Institutes of Biomedicine and HealthChinese Academy of SciencesGuangzhou510530China University of Chinese Academy of Sciences Beijing100049China Guangzhou Regenerative Medicine and Health Guangdong Laboratory(GRMH-GDL) Guangzhou510005China Institute for Stem cell and Regeneration Chinese Academy of SciencesBeijing100101China Research Unit of Generation of Large Animal Disease Models Chinese Academy of Medical Sciences(2019RU015)Guangzhou510530China School of Biotechnology and Health Sciences Wuyi UniversityJiangmen529020China Shenzhen Xenotransplantation Medical Engineering Research and Development Center Institute of Translational MedicineShenzhen University Health Science CenterShenzhen University School of MedicineFirst Affiliated Hospital of Shenzhen UniversityShenzhen Second People's HospitalShenzhen518035China Department of Central Laboratory Shenzhen Longhua District Central HospitalShenzhen518110China School of Life Sciences University of Science and Technology of ChinaHefei230027China Joint School of Life Sciences Guangzhou Institutes of Biomedicine and HealthChinese Academy of SciencesGuangzhou Medical UniversityGuangzhou511436China

Interspecies chimera through blastocyst complementation could be an alternative approach to create human organs in animals by using human pluripotent stem cells.A mismatch of the major histocompatibility complex of vascular endothelial cells between the human and host animal will cause graft rejection in the transplanted ***,to achieve a transplantable organ in animals without rejection,creation of vascular endothelial cells derived from humans within the organ is *** this study,to explore whether donor xeno-pluripotent stem cells can compensate for blood vasculature in host animals,we generated rat-mouse chimeras by injection of rat embryonic stem cells(rESCs)into mouse blastocysts with deficiency of Flk-1 protein,which is associated with endothelial and hematopoietic cell *** found that rESCs could differentiate into vascular endothelial and hematopoietic cells in the rat-mouse *** whole yolk sac(YS)of Flk-1^EGFP/ECFP rat-mouse chimera was full of rat blood *** genes related to vascular endothelial cells,arteries,and veins,blood vessels formation process,as well as hematopoietic cells,were highly expressed in the *** results suggested that rat vascular endothelial cells could undergo proliferation,migration,and self-assembly to form blood vasculature and that hematopoietic cells could differentiate into B cells,T cells,and myeloid cells in rat-mouse chimeras,which was able to rescue early embryonic lethality caused by Flk-1 deficiency in mouse.

关键词： Blastocyst complementation Interspecies chimera Intraspecies chimera Flk-1 vascular endothelial cell Hematopoietic cell

Anti-angiogenesis effect of generation 4 polyamidoamine/vascular endothelial growth factor antisense oligodeoxynucleotide on breast cancer in vitro

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2009年第3期10卷 159-167页

作者： Shan-zhi GU Xin-han ZHAO Ling-xiao ZHANG Li LI Zhi-yu WANG Min MENG Gai-li AN MOE Key Laboratory of Environment and Genes Related to Diseases Department of Medical Oncology the First Affiliated Hospital College of Medicine Xi'an Jiaotong University Xi 'an 710061 China

Objective:To study the effects of the generation 4 polyamidoamine/vascular endothelial growth factor antisense oligodeoxynucleotide(G4PAMAM/VEGFASODN) compound on the expressions of vascular endothelial growth factor(VEGF) and its mRNA of breast cancer cells and on the inhibition of vascular endothelial cells. Methods:We examined the morphology of G4PAMAM/VEGFASODN compound and its pH stability,in vitro transfection efficiency and toxicity,and the expressions of VEGF and its mRNA. Methyl thiazolyl tetrazolium assay was used to detect the inhibitory function of the compound on vascular endothelial cells. Results:The compound was about 10 nm in diameter and was homogeneously netlike. From pH 5 to 10,it showed quite a buffered ability. The 48-h transfection rate in the charge ratio of 1:40 was 98.76%,significantly higher than that of the liposome group(Pcells. The expressions of both VEGF protein and its mRNA after G4PAMAM/VEGFASODN transfection decreased markedly. Conclusion:With a low toxicity,high safety,and high transfection rate,G4PAMAM/VEGFASODN could be a promising gene vector. Specifically,it inhibits VEGF gene expression efficiently,laying a basis for further in vivo animal studies.

关键词： Breast cancer vascular endothelial growth factor (VEGF) VEGF mRNA Generation 4 polyamidoamine(G4PAMAM) Generation 4 polyamidoamine/vascular endothelial growth factor antisense oligodeoxynucleotide(G4PAMAM/VEGFASODN) vascular endothelial cell

Macrophage colony-stimulating factor expressed in non-cancer tissues provides predictive powers for recurrence in hepatocellular carcinoma

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World Journal of Gastroenterology 2016年第39期22卷 8779-8789页

作者： Hiroshi Kono Hideki Fujii Shinji Furuya Michio Hara Kazuyoshi Hirayama Yoshihiro Akazawa Yuuki Nakata Masato Tsuchiya Naohiro Hosomura Chao Sun First Department of Surgery Faculty of Medicine University of Yamanashi

AIM To investigate the role of macrophage colony-stimulating factor(M-CSF) in patients with hepatocellular carcinoma(HCC) after surgery. METHODS Expression of M-CSF, distribution of M2 macrophages(Mφs), and angiogenesis were assessed in the liver, including tumors and peritumoral liver tissues. The prognostic power of these factors was assessed. Mouse isolated hepatic Mφs or monocytes were cultured with media containing M-CSF. The concentration of vascular endothelial growth factor(VEGF) in media was assessed. Furthermore, the role of the M-CSF-matured hepatic Mφs on proliferation of the vascular endothelial cell(VEC) was investigated. RESULTS A strong correlation between the expressions of M-CSF and CD163 was observed in the peritumoral area. Also, groups with high density of M-CSF, CD163 or CD31 showed a significantly shorter time to recurrence(TTR) than low density groups. Multivariate analysis revealedthe expression of M-CSF or hepatic M2Mφs in the peritumoral area as the most crucial factor responsible for shorter TTR. Moreover, the expression of M-CSF and hepatic M2Mφs in the peritumoral area had better predictable power of overall survival. Values of VEGF in culture media were significantly greater in the hepatic Mφs compared with the monocytes. Proliferation of the VEC was greatest in the cells co-cultured with hepatic Mφs when M-CSF was present in *** M-CSF increases hepatocarcinogenesis, most likely by enhancing an angiogenic factor derived from hepatic Mφ and could be a useful target for therapy against HCC.

关键词： M2 macrophage vascular endothelial growth factor vascular endothelial cell Monocyte Angiogenesis

The Mechanical Study of vascular endothelial Growth Factor on the Prevention of Restenosis after Angioplasty

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2001年第3期21卷 195-197页

作者：刘启功陆再英周洪莲颜进张卫东 Department of Internal Medicine Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030

The mechanism of vascular endothelial growth factor (VEGF) on the prevention of restenosis after angioplasty was investigated. The cultured vascular endothelial cells (VEC) were incubated with the conditioned medium (CM) from vascular smooth muscle cells (VSMC) infected with recombinant adenoviruses containing the hVEGF 165 gene. To observe the effects of VEGF on proliferation and NO, ET, 6-keto-PGF1α secretion of VEC, WST-1 method, Griess method and radioimmunoassay were used respectively. The PDGF-B mRNA transcription in VECs was detected by RT-PCR. It was showed that NO, 6-keto-PGF1α and OD value were markedly increased in a dose-dependent manner in the VEGF-treated groups as compared with those in the control group, while ET and PDGF-B mRNA were significantly decreased in the VEGF-treated groups (P<0.05 or P<0.01). Adenovirus vector mediated hVEGF 165 gene could promote the proliferation of VECs and improve NO, PGI 2 secretion, inhibit ET secretion and PDGF-B mRNA transcription in the VECs. The above results offered further theoretical evidence for VEGF on the prevention of restenosis after angioplasty.

关键词： vascular endothelial growth factor adenovirus gene therapy vascular endothelial cell restenosis

HEPATOCYTE GROWTH FACTOR PROTECTS AGAINST APOPTOSIS INDUCED BY ADVANCED GLYCATION END PRODUCTS IN endothelial cellS

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Chinese Medical Sciences Journal 2006年第1期21卷 6-10页

作者： Yi-jun Zhou Jia-he Wang Jin Zhang Department of Endocrinology and Metabolism China Medical University Shenyang 110001 Department of Infectious Diseases the First Affiliated Hospital China Medical University Shenyang 110001

Objective To investigate the effects of hepatocyte growth factor(HGF)on vascular endothelial cells apoptosis induced by advanced glycation end products(AGEs)and its possible mechanism. Methods Human umbilical vein endothelial cells(HUVECs)were cultured in vitro and intervened by different concentrations of AGEs and *** cell inhibitory rates of each group with different culture time(12, 24, 48, and 72 hours)were measured by methyl thiazolyl tetrazolium(MTT)assay. The early stage apoptosis was detected by flow cytometry with Annexin V-FITC/PI double staining, morphology of cell apoptosis was observed by hoechst 33258 fluorescence staining, and the expression of apoptosis-associated genes Bax and Bcl-2 were determined by Western *** activity of caspase-3 was detected by enzyme-linked immunosorbent assay (ELISA).Results Morphological observation indicated that high concentration of AGEs induced characteristic apoptotic changes in *** a certain concentration range, HUVECs apoptosis inducing rates by AGEs were in both dose- and time-dependent *** significantly inhibited the apoptosis of HUVECs induced by AGEs (Pendothelial cells in *** may effectively attenuate AGEs-induced endothelial cells apoptosis through upregulating Bcl-2 gene expression and inhibiting caspase-3 activation.

关键词： hepatocyte growth factor advanced glycation end products vascular endothelial cell apoptosis atherosclerosis