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Acta Biochimica et Biophysica Sinica 2004年第12期36卷 845-850页

作者： Hou, Wei-Hong Wagn, Tian-Yun Yuan, Bao-Mei Chai, Yu-Rong Jia, Yan-Long Tian, Fang Wang, Jian-Min Xue, Le-Xun Laboratory for cell biology Zhengzhou UniversityZhengzhou 450052 China

Human canstatin, a 24 kD fragment of the α2 chain of type IV collagen, has been proved to be one of the most effective inhibitors of angiogenesis and tumor growth. To investigatein vivoantiangiogenesis activity andin vitroeffects on endothelial cell proliferation of recombinant mouse canstatin, the cDNA of mouse canstatin was introduced into an expression vector pQE40 to construct a prokaryotic expression vector pQE-mCan. The recombinant mouse canstatin efficiently expressed inE. coliM15 after IPTG induction was monitored by SDS-PAGE and by Western blotting with an anti-hexahistidine tag antibody. The expressed mouse canstatin, mainly as inclusion bodies, accounted for approximately 35% of the total bacterial proteins. The inclusion bodies were washed, lysed and purified by the nickel affinity chromatography to a purity of approximately 93%. The refolded mouse canstatin was tested on the chicken embryo chorioallantoic membranes (CAM), and a large number of newly formed blood vessels were significantly regressed. In addition, recombinant mouse canstatin potently inhibited endothelial cell proliferation with no inhibition on non-endothelial cells. Taken together, these findings demonstrate that the recombinant mouse canstatin effectively inhibited angiogenesis of the chicken embryo in a dose-dependent manner and specially suppressed in vitro the proliferation of human umbilical vein endothelial cells.

关键词： mouse canstatin angiogenesis inhibitor prokaryotic expression

Resident endothelial cells generate hepatocytes through cell fusion in adult mouse liver

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Journal of Genetics and Genomics 2020年第4期47卷 225-228页

作者： Wenjuan Pu Ximeng Han Mingjun Zhang Yan Li Xiuzhen Huang Lingjuan He Bin Zhou State Key Laboratory of cell biology Shanghai Institute of Biochemistry and Cell BiologyCenter for Excellence in Molecular Cell ScienceChinese Academy of SciencesShanghai 200031China University of Chinese Academy of Sciences Beijing 100049China State Key Laboratory of cell biology Shanghai Institute of Biochemistry and Cell BiologyCenter for Excellence in Molecular Cell ScienceChinese Academy of SciencesUniversity of Chinese Academy of SciencesShanghai 200031China School of Life Science and Technology ShanghaiTech UniversityShanghai 201210China

Unravelling lineage plasticity and cellular contribution to hepatocytes provides valuable information for understanding sources that fuel homeostatic renewal of the liver(Miyajima et al.,2014).In the adult stage,hepatocytes are mainly self-renewed through cell division(Schaub et al.,2014;Tarlow et al.,2014;Yanger et al.,2014).Under severe injury or when hepatocyte proliferation is significantly impaired,cholangiocytes or biliary epithelial cells contribute to hepatocytes(Raven et al.,2017;Deng et al.,2018).

关键词： liver impaired

Expression of vascular endothelial growth factor-C and angiogenesis in esophageal squamous cell carcinoma

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World Journal of Gastroenterology 2006年第28期12卷 4582-4585页

作者： Ming-Xing Ding Xing-Qiu Lin Xiao-Yan Fu Ning Zhang Ji-Cheng Li School of Medicine Jinhua College of Profession & Technology Jinhua 321007 Zhejiang Province China Institute of cell biology Zhejiang University Hangzhou 310031 Zhejiang Province China

AIM： To investigate the expression of vascular endothelial growth factor-c （VEGF-C） mRNA and microvessel density （MVD） in human esophageal squamous cell carcinoma （ESCC） and its relationship with clinical significance. METHODS： Specimens obtained from 43 patients undergoing surgical resection for ESCC were used in this study. The expression of VEGF-C mRNA was examined by in situ hybridization. Tumor MVD was determined immunohistochemically with anti-CD31 antibody and estimated by image analysis. Ten sections of adjacent normal mucosa were also examined. RESULTS： VEGF-C mRNA expression was detected in cytoplasm of carcinoma cells. Of the 43 ESCC patients studied, 18 cases （41.9%） were positive for VEGF-C mRNA. No VEGF-C mRNA expression was observed in normal esophageal mucosa. VEGF-C mRNA expression correlated significantly with lymph node metastasis, TNM stage and depth of invasion （P 〈 0.05）. Furthermore, histological grade （differentiation） tended to correlate with VEGF-C mRNA expression, but was not statistically significant （P 〉 0.05）. In tumor lesions, the MVD was significantly greater than that in normal esophageal mucosa. MVD correlated significantly with lymph node metastasis, TNM stage and depth of invasion （P 〈 0.05）, but not with histological grade （differentiation）（P 〉 0.05）. Lesions with VEGF-C mRNA expression had a significantly higher MVD than that of those without VEGF-C mRNA expression （P 〈 0.05）. CONCLUSION： VEGF-C plays a role in lymphatic metastasis via lymphangiogenesis and angiogenesis in ESCC. VEGF-C is one of the important predictors of the biological behavior in ESCC.

关键词： Vascular endothelial growth factor-c Esophageal carcinoma Angiogenesis Microvessel density Lymph node metastasis In situ hybridization

Mesenchymal stem cell-derived small extracellular vesicles mitigate oxidative stress-induced senescence in endothelial cells via regulation of miR-146a/Src

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Signal Transduction and Targeted Therapy 2021年第11期6卷 3318-3332页

作者： Xian Xiao Meiqian Xu Hongliang Yu Liping Wang Xiaoxia Li Janusz Rak Shihua Wang Robert Chunhua Zhao Institute of Basic Medical Sciences Chinese Academy of Medical Sciences School of Basic Medicine Peking Union Medical CollegeBeijingChina Department of Genetics and cell biology Basic medical collegeQingdao University308 Ningxia Road266071QingdaoChina Research Institute of the McGill University Health Centre Glen SiteMcGill UniversityMontrealQCH4A 3J1Canada Department of cell biology School of Life SciencesShanghai University200444ShanghaiChina

Senescent endothelial cells (ECs) could impair the integrity of the blood vessel endothelium, leading to vascular aging and a series of diseases, such as atherosclerosis, diabetes. Preventing or mitigating EC senescence might serve as a promising therapeutic paradigm for these diseases. Recent studies showed that small extracellular vesicles (sEV) have the potential to transfer bioactive molecules into recipient cells and induce phenotypic changes. Since mesenchymal stem cells (MSCs) have long been postulated as an important source cell in regenerative medicine, herein we investigated the role and mechanism of MSC-derived sEV (MSC-sEV) on EC senescence. In vitro results showed that MSC-sEV reduced senescent biomarkers, decreased senescence-associated secretory phenotype (SASP), rescued angiogenesis, migration and other dysfunctions in senescent EC induced by oxidative stress. In the In vivo natural aging and type-2 diabetes mouse wound-healing models (both of which have senescent ECs), MSC-sEV promoted wound closure and new blood vessel formation. Mechanically, miRNA microarray showed that miR-146a was highly expressed in MSC-sEV and also upregulated in EC after MSC-sEV treatment. miR-146a inhibitors abolished the stimulatory effects of MSC-sEV on senescence. Moreover, we found miR-146a could suppress Src phosphorylation and downstream targets VE-cadherin and Caveolin-1. Collectively, our data indicate that MSC-sEV mitigated endothelial cell senescence and stimulate angiogenesis through miR-146a/Src.

关键词： miR wound healing

Bridging long gap peripheral nerve injury using skeletal muscle-derived multipotent stem cells

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Neural Regeneration Research 2014年第14期9卷 1333-1336页

作者： Tetsuro Tamaki Muscle Physiology & cell biology unit Department of Regenerative MedicineDivision of Basic Clinical ScienceTokai University School of Medicine Isehara Japan

Long gap peripheral nerve injuries usually reulting in life-changing problems for patients. Skeletal muscle derived-multipotent stem cells （Sk-MSCs） can differentiate into Schwann and perineurial/endoneurial cells, vascular relating pericytes, and endothelial and smooth muscle cells in the damaged peripheral nerve niche. Application of the Sk-MSCs in the bridging conduit for repairing long nerve gap injury resulted favorable axonal regeneration, which showing superior effects than gold standard therapy--healthy nerve autograft. This means that it does not need to sacrifice of healthy nerves or loss of related functions for repairing peripheral nerve injury.

关键词： peripheral nerve support cells Schwann cells perineurium endoneurium cytokine,paracrine effect blood vessel formation

Expression of Vascular endothelial Growth Factor-C and Vascular endothelial Growth Factor Receptor-3 in Ovarian Epithelial Tumors

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Chinese Journal of Cancer Research 2007年第2期19卷 124-130页

作者：傅晓艳丁明星张宁林兴秋李继承 School of Medicine Jinhua College of Profession & Technology Institute of cell biology Zhejiang University

Objective： To explore the role of vascular endothelial growth factor-C （VEGF-C） in the process of angiogenesis, lymphangiogenesis and lymphatic metastasis in epithelial ovarian tumors. Methods： In situ hybridization and immunohistochemical staining for VEGF-C were performed in 30 epithelial ovarian carcinomas, 9 borderline tumors and 26 benign tumors. endothelial cells were immunostained with anti-VEGFR-3 pAb and anti-CD31 mAb, and VEGFR-3 positive vessels and microvessel density （MVD） were assessed by image analysis. Results： VEGF-C mRNA and protein expression were detected in cytoplasm of carcinoma cells. VEGF-C mRNA and protein expression in ovarian epithelial carcinomas were significantly higher than those in borderline tumors and benign tumors （P〈0.05 or P〈0.01）. In ovarian epithelial carcinomas, VEGF-C protein expression, VEGFR-3 positive vessels and MVD were significantly higher in the cases of clinical stage Ⅲ-Ⅳ and with lymph node metastasis than those of clinical stage Ⅰ-Ⅱ and without lymph node metastasis respectively （P〈0.05 or P〈0.01）. VEGFR-3 positive vessels and MVD were significantly higher in VEGF-C protein positive tumors than negative tumors （P〈0.05）. VEGFR-3 positive vessels was significantly correlated with MVD（P〈0.01）. Conclusion： VEGF-C might play a role in lymphatic metastasis via lymphangiogenesis and angiogenesis in epithelial ovarian tumors, and VBEGF-C could be used as a biologic marker of metastasis in ovarian epithelial tumors.

关键词： Ovarian neoplasms Vascular endothelial growth factor-c (VEGF-C) VEGF receptor-3(VEGFR-3) CD 31 Metastasis

endothelial progenitor cell transplantation ameliorates elastin breakdown in a Kawasaki disease mouse model

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Chinese Medical Journal 2012年第13期125卷 2295-2301页

作者： CHEN Zhi DU Zhong-dong LIU Jun-feng LU Dun-xiang LI Li GUAN Yun-qian WAN Sui-gui Department of Pediatrics Beijing Children's Hospital CapitalMedical University Beijing 100045 China Laboratory of cell biology Xuanwu Hospital Capital Medical University Beijing 100053 China

Background Coronary artery damage from Kawasaki disease （KD） is closely linked to the dysfunction of endothelial progenitor cells （EPCs）. The aim of the present study was to evaluate the therapeutic effect of EPCs transplantation in KD model. Methods Lactobacillus casei cell wall extract （LCWE）-induced KD model in C57BL/6 mice was established. The model mice were injected intravenously with bone marrow-derived in vitro expanded EPCs. Histological evaluation, number of circulating EPCs and the function of bone marrow EPCs were examined at day 56. Results Inflammation was found around the coronary artery of the model mice after 14 days, Elastin breakdown was observed after 56 days. CM-Dil labeled EPCs incorporated into vessel repairing foci was found. At day 56, the number of peripheral EPCs in the KD model group was lower than in EPCs transplanted and control group. The functional index of bone marrow EPCs from the KD model group decreased in proliferation, adhesion and migration. Increased number of circulating EPCs and improved function were observed on the EPCs transplanted group compared with model group. Conclusion Exogenously administered EPCs, which represent a novel strategy could prevent the dysfunction of EPCs, accelerate the repair of coronary artery endothelium lesion and decrease the occurrence of aneurysm.

关键词： Kawasaki disease endothelial progenitor cell transplantation mouse model

Regulation of tumor angiogenesis by the microtubule-binding protein CLIP-170

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Protein & cell 2013年第4期4卷 266-276页

作者： Xiaodong Sun Fang Li Bin Dong Shaojun Suo Min Liu Dengwen Li Jun Zhou Department of Genetics and cell biology College of Life SciencesNankai UniversityTianjin 300071China

Angiogenesis,the expansion of preexisting blood vessels,is a complex process required for tumor growth and *** current antiangiogenic strategies have shown promising results in several cancer types,identification of additional antiangiogenic targets is required to improve the therapeutic ***,we show that the microtubule-binding protein CLIP-170(cytoplasmic linker protein of 170 kDa)is highly expressed in breast tumor samples and correlates positively with blood vessel *** of CLIP-170 signifi cantly impaired vascular endothelial tube formation and sprouting in vitro and inhibited breast tumor growth in mice by decreasing tumor *** data further show that CLIP-170 is important for the migration but not the proliferation of vascular endothelial *** addition,CLIP-170 promotes the polarization of endothelial cells in response to the angiogenic *** fi ndings thus demonstrate a critical role for CLIP-170 in tumor angiogenesis and suggest its potential as a novel antiangiogenic target.

关键词： tumor angiogenesis endothelial cell migration polarization microtubule

Future options of anti-angiogenic cancer therapy

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Chinese Journal of Cancer 2016年第2期35卷 88-96页

作者： Yihai Cao Department of Microbiology Tumor and Cell BiologyKarolinska Institute Department of Medical and Health Sciences Linkoping University Department of Cardiovascular Sciences University of Leicester and NIHR Leicester Cardiovascular Biomedical Research UnitGlenfield Hospital

In human patients,drugs that block tumor vessel growth are widely used to treat a variety of cancer *** rigorous phase 3 clinical trials have demonstrated significant survival benefits;however,the addition of an anti-angiogenic component to conventional therapeutic modalities has generally produced modest survival benefits for cancer ***,it is unclear why these clinically available drugs targeting the same angiogenic pathways produce dissimilar effects in preclinical models and human *** this article,we discuss possible mechanisms of various anti-angiogenic drugs and the future development of optimized treatment regimens.

关键词： Angiogenesis, Cancer therapy, Anti-angiogenesis, Vascular endothelial growth factor, Biomarker

endothelial progenitor cell down-regulation in a mouse model of Kawasaki disease

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Chinese Medical Journal 2012年第3期125卷 496-501页

作者： LIU Jun-feng DU Zhong-dong CHEN Zhi LU Dun-xiang LI Li GUAN Yun-qian WAN Sui-gui Department of Pediatrics Beijing Children's Hospital Capital Medical University Beijing 100045 China Laboratory of cell biology Xuanwu Hospital Capital Medical University Beijing 100053 China

Background Cardiovascular complications of Kawasaki disease （KD） are a common cause of heart disease in pediatric *** studies have suggested a role for endothelial progenitor cells （EPCs） in coronary artery lesions associated with ***,long-term observations of EPCs during the natural progression of this disorder are *** an experimental model of KD,we aimed to determine whether the coronary artery lesions are associated with down-regulation of *** To induce KD,C57BL/6 mice were administered an intraperitoneal injection of Lactobacillus casei cell wall extract （LCWE; phosphate buffered saline used as control vehicle）.Study groups included：group A （14 days following LCWE injection）,group B （56 days following LCWE injection） and group C （controls）.Numbers of circulating EPCs （positively staining for both CD34 and FIk-1 while staining negative for CD45） were evaluated using flow *** marrow mononuclear cells were cultured in vitro to expand EPCs for functional *** vitro EPC proliferation,adhesion and migration were *** The model was shown to exhibit similar coronary artery lesions to KD patients with coronary *** of circulating EPCs decreased significantly in the KD models （groups A and B） compared to controls （（0.017±0.008）% VS.（0.028±0.007）%,P〈0.05 and （0.016±0.007）% vs.（0.028±0.007）%,P 〈0.05）.Proliferative,adhesive and migratory properties of EPCs were markedly impaired in groups A and *** Coronary artery lesions in KD occur as a consequence of impaired vascular injury repair,resulting from excess consumption of EPCs together with a functional impairment of bone marrow EPCs and their precursors.

关键词： Kawasaki disease endothelial progenitor cells coronary aneurysm mouse model