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World Journal of Gastroenterology 2022年第3期28卷 275-289页

作者： Andrzej S Tarnawski Amrita Ahluwalia Gastroenterology Research Department University of California Irvine and the Veterans Administration Long Beach Healthcare SystemLong BeachCA 90822United States Research Service Veterans Administration Long Beach Healthcare SystemLong BeachCA 90822United States

The coronavirus disease 2019(COVID-19)infected so far over 250 million people and caused the death of over 5 million worldwide.Aging,diabetes,and cardiovascular diseases,conditions with preexisting impaired endothelial functions predispose to COVID-19.While respiratory epithelium is the main route of virus entry,the endothelial cells(ECs)lining pulmonary blood vessels are also an integral part of lung injury in COVID-19 patients.COVID-19 not only affects the lungs and respiratory system but also gastrointestinal(GI)tract,liver,pancreas,kidneys,heart,brain,and skin.Blood vessels are likely conduits for the virus dissemination to these distant organs.Importantly,ECs are also critical for vascular regeneration during injury/lesions healing and restoration of vascular network.The World Journal of Gastroenterology has published in last two years over 67 outstanding papers on COVID-19 infection with a focus on the GI tract,liver,pancreas,etc.,however,the role of the endothelial and vascular components as major targets for COVID-19-induced tissue injury,spreading to various organs,and injury healing have not been sufficiently emphasized.In the present article,we focus on these subjects and on current treatments including the most recent oral drugs molnupiravir and paxlovid that show a dramatic,significant efficacy in controlling severe COVID-19 infection.

关键词： endothelial cells Impaired endothelial function Blood vessels SARS-CoV-2 COVID-19 Cytokine storm

Thinking outside the black box:are the brain endothelial cells the new main target in Alzheimer's disease?

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Neural Regeneration Research 2023年第12期18卷 2592-2598页

作者： Enrique Estudillo Adolfo López-Ornelas Alejandro Rodríguez-Oviedo Neptali Gutiérrez de la Cruz Marco Antonio Vargas-Hernández Adriana Jiménez Laboratorio de Reprogramación Celular Instituto Nacional de Neurología y Neurocirugía Manuel Velasco SuárezMexico CityMexico División de Investigación Hospital Juárez de MéxicoMexico CityMexico Hospital Nacional Homeopático Hospitales Federales de ReferenciaMexico CityMexico Facultad de Ciencias Universidad Nacional Autónoma de MéxicoMexico CityMexico Laboratorio de Morfología Escuela Militar de Graduados de SanidadSecretaría de la Defensa NacionalBatalla de CelayaLomas de SoteloMiguel HidalgoMexico CityMexico Escuela Militar de Graduados de Sanidad Secretaría de la Defensa NacionalBatalla de CelayaLomas de SoteloMiguel HidalgoMexico CityMexico

The blood-brain barrier is the interface through which the brain interacts with the milieu and consists mainly of a sophisticated network of brain endothelial cells that forms blood vessels and selectively moves molecules inside and outside the brain through multiple mechanisms of transport.Although brain endothelial cell function is crucial for brain homeostasis,their role in neurodegenerative diseases has historically not been considered with the same importance as other brain cells such as microglia,astroglia,neurons,or even molecules such as amyloid beta,Tau,or alpha-synuclein.Alzheimer's disease is the most common neurodegenerative disease,and brain endothelial cell dysfunction has been reported by several groups.However,its impairment has barely been considered as a potential therapeutic target.Here we review the most recent advances in the relationship between Alzheimer's disease and brain endothelial cells commitment and analyze the possible mechanisms through which their alterations contribute to this neurodegenerative disease,highlighting their inflammatory phenotype and the possibility of an impaired secretory pattern of brain endothelial cells that could contribute to the progression of this ailment.Finally,we discuss why shall brain endothelial cells be appreciated as a therapeutic target instead of solely an obstacle for delivering treatments to the injured brain in Alzheimer's disease.

关键词： dementia endothelial cells neurodegeneration neuroinflammation neuronal death paracellular transport transcellular transport

The relationship between amyloid-beta and brain capillary endothelial cells in Alzheimer's disease

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Neural Regeneration Research 2022年第11期17卷 2355-2363页

作者： Yan-Li Zhang Juan Wang Zhi-Na Zhang Qiang Su Jun-Hong Guo Department of Neurology First Hospital of Shanxi Medical UniversityTaiyuanShanxi ProvinceChina Department of Neurology Sixth Hospital of Shanxi Medical University(General Hospital of Tisco)TaiyuanShanxi ProvinceChina School of Public Health Shanxi Medical UniversityTaiyuanShanxi ProvinceChina

Neurovascular dysfunction,as an integral part of Alzheimer's disease,may have an important influence on the onset and progression of chronic neurodegenerative processes.The bloodbrain barrier(BBB)pathway is one of the main pathways that mediates the clearance of amyloidbeta(Aβ)in the brain parenchyma.A large number of studies have shown that receptors and ATPbinding cassette transporte rs expressed on endothelial cells play an important role in Aβtransport across the BBB,but the specific mechanism is not clear.In this review,we summarize the possible mechanisms of Aβproduction and clearance,and in particular the relationship between Aβand brain capillary endothelial cells.Aβis produced by abnormal cleavage of the amyloid precursor protein via amyloidogenic processing under pathological conditions.Dys regulation of Aβclearance is considered to be the main reason for the massive accumulation of Aβin the brain parenchyma.Several pathways mediating Aβclearance from the brain into the periphery have been identified,including the BBB pathway,the blood-cerebros pinal fluid barrier and arachnoid granule pathway,and the lymphoidrelated pathway.Brain ca pilla ry endothelial cells are the key components of Aβclearance mediated by BBB.Receptors(such as LRP1,RAGE,and FcRn)and ATP-binding cassette transporters(such as P-gp,ABCA1,and ABCC1)expressed on endothelial cells play a critical role in Aβtranscytosis across the BBB.The toxic effects of Aβcan induce dysregulation of receptor and transpo rter expression on endothelial cells.Excessive Aβexerts potent detrimental cerebrovascular effects by promoting oxidative stress,inducing chronic inflammation,and impairing endothelial structure and functions.All of these are main causes for the reduction in Aβclearance across the BBB and the accumulation of Aβin the brain parenchyma.Therefo re,studies on the intera ctions between Aβand brain capillary endothelial cells,including their receptors and transporters,studies on inhibition of the toxic effects of Aβon endothelial cells,and stud

关键词： Alzheimer's disease amyloid beta Aβclearance blood-brain barrier cerebral amyloid angiopathy dementia endothelial cells oxidative stress review therapeutics transcytosis

A new hemostatic agent composed of Zn^(2+)-enriched Ca^(2+)alginate activates vascular endothelial cells in vitro and promotes tissue repair in vivo

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Bioactive Materials 2022年第12期7卷 368-382页

作者： Anne-Charlotte Ponsen Richard Proust Sabrina Soave Françoise Mercier-Nom´e Isabelle Garcin Laurent Combettes Jean-Jacques Lataillade Georges Uzan INSERM UMRS-MD 1197 Universit´e Paris-SaclayInstitut Andr´e LwoffHˆopital Paul BrousseVillejuifFrance Plateforme d’Histologie Immunopathologie de Clamart(PHIC) Universit´e Paris-SaclayINSERMCNRSInstitut Paris Saclay d’Innovation Th´erapeutiqueChˆatenay-MalabryFrance Universit´e Paris-Saclay INSERMInflammationMicrobiome and ImmunosurveillanceClamartFrance INSERM UMRS 1174 Universit´e Paris-SaclayOrsayFrance Centre de Transfusion Sanguine des Arm´ees ClamartFrance

To control capillary bleeding, surgeons may use absorbable hemostatic agents, such as Surgicel® and TachoSil®. Due to their slow resorption, their persistence in situ can have a negative impact on tissue repair in the resected organ. To avoid complications and obtain a hemostatic agent that promotes tissue repair, a zinc-supplemented calcium alginate compress was developed: HEMO-IONIC®. This compress is non-absorbable and is therefore removed once hemostasis has been achieved. After demonstrating the hemostatic efficacy and stability of the blood clot obtained with HEMO-IONIC, the impact of Surgicel, TachoSil, and HEMO-IONIC on cell activation and tissue repair were compared (i) in vitro on endothelial cells, which are essential to tissue repair, and (ii) in vivo in a mouse skin excision model. In vitro, only HEMO-IONIC maintained the phenotypic and functional properties of endothelial cells and induced their migration. In comparison, Surgicel was found to be highly cytotoxic, and TachoSil inhibited endothelial cell migration. In vivo, only HEMO-IONIC increased angiogenesis, the recruitment of cells essential to tissue repair (macrophages, fibroblasts, and epithelial cells), and accelerated maturation of the extracellular matrix. These results demonstrate that a zinc-supplemented calcium alginate, HEMO-IONIC, applied for 10 min at the end of surgery and then removed has a long-term positive effect on all phases of tissue repair.

关键词： Hemostatic agent Alginate Surgery Hemostasis endothelial cells Tissue repair

Overexpression of mitogen-activated protein kinase phosphatase-1 in endothelial cells reduces blood-brain barrier injury in a mouse model of ischemic stroke

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Neural Regeneration Research 2023年第8期18卷 1743-1749页

作者： Xiu-De Qin Tai-Qin Yang Jing-Hui Zeng Hao-Bin Cai Shao-Hua Qi Jian-Jun Jiang Ying Cheng Long-Sheng Xu Fan Bu Department of Neurology&Psychology Shenzhen Traditional Chinese Medicine HospitalThe Fourth Clinical Medical College of Guangzhou University of Chinese MedicineShenzhenGuangdong ProvinceChina Department of Cardiothoracic Surgery Shenzhen Traditional Chinese Medicine HospitalThe Fourth Clinical Medical College of Guangzhou University of Chinese MedicineShenzhenGuangdong ProvinceChina Department of Neurology The University of Texas Health Science Center at HoustonHoustonTXUSA Department of Nephrology Shenzhen Traditional Chinese Medicine HospitalThe Fourth Clinical Medical College of Guangzhou University of Chinese MedicineShenzhenGuangdong ProvinceChina Department of Anesthesiology and Pain Medicine The Affiliated Hospital of Jiaxing UniversityJiaxingZhejiang ProvinceChina

Ischemic stroke can cause blood-brain barrier(BBB)injury,which worsens brain damage induced by stroke.Abnormal expression of tight junction proteins in endothelial cells(ECs)can increase intracellular space and BBB leakage.Selective inhibition of mitogen-activated protein kinase,the negative regulatory substrate of mitogen-activated protein kinase phosphatase(MKP)-1,improves tight junction protein function in ECs,and genetic deletion of MKP-1 aggravates ischemic brain injury.However,whether the latter affects BBB integrity,and the cell type-specific mechanism underlying this process,remain unclear.In this study,we established an adult male mouse model of ischemic stroke by occluding the middle cerebral artery for 60 minutes and overexpressed MKP-1 in ECs on the injured side via lentiviral transfection before stroke.We found that overexpression of MKP-1 in ECs reduced infarct volume,reduced the level of inflammatory factors interleukin-1β,interleukin-6,and chemokine C-C motif ligand-2,inhibited vascular injury,and promoted the recovery of sensorimotor and memory/cognitive function.Overexpression of MKP-1 in ECs also inhibited the activation of cerebral ischemia-induced extracellular signal-regulated kinase(ERK)1/2 and the downregulation of occludin expression.Finally,to investigate the mechanism by which MKP-1 exerted these functions in ECs,we established an ischemic stroke model in vitro by depriving the primary endothelial cell of oxygen and glucose,and pharmacologically inhibited the activity of MKP-1 and ERK1/2.Our findings suggest that MKP-1 inhibition aggravates oxygen and glucose deprivation-induced cell death,cell monolayer leakage,and downregulation of occludin expression,and that inhibiting ERK1/2 can reverse these effects.In addition,co-inhibition of MKP-1 and ERK1/2 exhibited similar effects to inhibition of ERK1/2.These findings suggest that overexpression of MKP-1 in ECs can prevent ischemia-induced occludin downregulation and cell death via deactivating ERK1/2,thereby protecting the integrity of BBB

关键词： blood-brain barrier brain injury cerebral ischemia endothelial cells extracellular signal-regulated kinase 1/2 functional recovery mitogenactivated protein kinase phosphatase 1 occludin oxygen and glucose deprivation transient middle cerebral artery occlusion

Effect of VEGF/GREDVY Modified Surface on Vascular cells Behavior

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Journal of Wuhan University of Technology(Materials Science) 2024年第1期39卷 244-254页

作者：魏来 TAN Jianying LI Li WANG Huanran LIU Sainan ZENG Zheng LIU Tao WANG Jian 陈俊英 WENG Yajun School of Materials Science and Engineering Southwest Jiaotong UniversityChengdu 610031 China

We synthesized B-He/B-GREDVY and immobilized them on avidin-coated surfaces.To examine the immobilization of molecules in the material, the following experiments were performed:fluorescein isothiocyanate(FITC) fluorescence staining, water contact angle and atomic force microscopy(AFM) measurements. Besides, the biological evaluation experiments were also performed, such as platelets adhesion and activation, the culturing of smooth muscle cells(SMC) and endothelial cells(EC). These experimental results show that the modified surfaces could prevent the hyperproliferation of SMC, and promote the proliferation and migration of EC and EPC. Furthermore, the adding of VEGF improved the EC adhesion in a dynamic environment. Generally, it is expected that the modified surfaces could be used to accelerate the formation of the newly endothelial layer for the construction of platforms for coronary artery stent therapy.

关键词： biotin-GREDVY VEGF anticoagulation endothelial cells endothelial progenitor cells

Advances in the differentiation of pluripotent stem cells into vascular cells

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World Journal of Stem cells 2024年第2期16卷 137-150页

作者： Yi-Chang Jiao Ying-Xin Wang Wen-Zhu Liu Jing-Wen Xu Yu-Ying Zhao Chuan-Zhu Yan Fu-Chen Liu Department of Neurology Qilu Hospital of Shandong UniversityJinan 250012Shandong ProvinceChina Research Institute of Neuromuscular and Neurodegenerative Diseases Qilu Hospital of Shandong UniversityJinan 250012Shandong ProvinceChina Mitochondrial Medicine Laboratory Qilu Hospital(Qingdao)of Shandong UniversityQingdao 266103Shandong ProvinceChina Brain Science Research Institute Shandong UniversityJinan 250012Shandong ProvinceChina

Blood vessels constitute a closed pipe system distributed throughout the body,transporting blood from the heart to other organs and delivering metabolic waste products back to the lungs and kidneys.Changes in blood vessels are related to many disorders like stroke,myocardial infarction,aneurysm,and diabetes,which are important causes of death worldwide.Translational research for new appro-aches to disease modeling and effective treatment is needed due to the huge socio-economic burden on healthcare systems.Although mice or rats have been widely used,applying data from animal studies to human-specific vascular physiology and pathology is difficult.The rise of induced pluripotent stem cells(iPSCs)provides a reliable in vitro resource for disease modeling,regenerative medicine,and drug discovery because they carry all human genetic information and have the ability to directionally differentiate into any type of human cells.This review summarizes the latest progress from the establishment of iPSCs,the strategies for differentiating iPSCs into vascular cells,and the in vivo trans-plantation of these vascular derivatives.It also introduces the application of these technologies in disease modeling,drug screening,and regenerative medicine.Additionally,the application of high-tech tools,such as omics analysis and high-throughput sequencing,in this field is reviewed.

关键词： Induced pluripotent stem cell Blood vessels Vascular organoids endothelial cells Smooth muscle cells Pericytes Tissue engineering vascular graft

Induced migration of endothelial cells into 3D scaffolds by chemoattractants secreted by pro-inflammatory macrophages in situ

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Regenerative Biomaterials 2017年第3期4卷 139-148页

作者： Xuguang Li Yuankun Dai Tao Shen Changyou Gao MOE Key Laboratory of Macromolecular Synthesis and Functionalization Department of Polymer Science and EngineeringZhejiang UniversityHangzhou 310027China

Cell migration in scaffolds plays a crucial role in tissue regeneration,which can better mimic cell behaviors in vivo.In this study,a novel model has been proposed on controlling 3D cell migration in porous collagen-chitosan scaffolds with various pore structures under the stimulation of inflammatory cells to mimic the angiogenesis process.endothelial cells(ECs)cultured atop the scaffolds in the Transwell molds which were placed into a well of a 24-well culture plate were promoted to migrate into the scaffolds by chemoattractants such as vascular endothelial growth factor(VEGF)and tumor necrosis factor-alpha(TNF-α)secreted by the pro-inflammatory macrophages incubated in the well culture plate.The phenotype of macrophages was mediated by 50 ng/ml interferongamma(IFN-c)and different concentrations of lipopolysaccharide(LPS,150–300 ng/ml).The cell migration depth had a positive correlation with LPS concentration,and thereby the TNF-a concentration.The ECs migrated easier to a deeper zone of the scaffolds prepared at10C(187 lm in pore diameter)than that at20C(108 lm in pore diameter)as well.The method provides a useful strategy to study the 3D cell migration,and is helpful to reveal the vascularization process during wound healing in the long run.

关键词： cell migration chemoattractants endothelial cells macrophages scaffolds

Cytotoxic effects of docetaxel as a candidate drug of drug-eluting stent on human umbilical vein endothelial cells and the signaling pathway of cell migration inhibition,adhesion delay and shape change

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Regenerative Biomaterials 2017年第3期4卷 167-178页

作者： Tingzhang Hu Chun Yang Meiling Fu Jiali Yang Rolin Du Xiaolin Ran Tieying Yin Guixue Wang Key Laboratory for Biorheological Science and Technology of Ministry of Education State and Local Joint Engineering Laboratory for Vascular ImplantsBioengineering College of Chongqing UniversityChongqing 400030China

Docetaxel(DTX),a paclitaxel analogue,can efficiently inhibit proliferation of vascular smooth muscle cells and has broadly been used as an antiangiogenesis drug.However,as a candidate drug of drug-eluting stent,the effects of DTX on human umbilical vein endothelial cells(HUVECs)are still not well understood.Herein,we investigated the effects of DTX on proliferation,apoptosis,adhesion,migration and morphology of HUVECs in vitro.We found that DTX had the cytostatic and cytotoxic effects at low and high concentrations,respectively.DTX could inhibit the proliferation and migration of HUVECs,induce HUVECs apoptosis,delay HUVECs adhesion and decrease spreading area and aspect ratio of individual cells.The signaling pathway that DTX led to the migration inhibition,adhesion delay and shape change of HUVECs is the VE-cadherin mediated integrin b1/FAK/ROCK signaling pathway.The study will provide a theoretical basis for the clinical application of DTX.

关键词： cytotoxic effects docetaxel endothelial cells signaling pathway

Morroniside protects cultured human umbilical vein endothelial cells from damage by high ambient glucose

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Acta Pharmacologica Sinica 2004年第4期25卷 14-17页

作者： Hui-qin XU2, Hai-ping HAO2, Xu ZHANG3,Yang PAN2 2College of Pharmacy 3BasicMedicine College, Nanjing Universityof Traditional ChineseMedicine, Nanjing 210029, China College of Pharmacy Nanjing University of Traditional Chinese Medicine Nanjing 210029 Basic Medicine College Nanjing University of Traditional Chinese Medicine Nanjing 210029

AIM: To determine whether morroniside, a compound in Cornus officinalis Sieb et Zucc can prevent cultured human umbilical vein endothelial cells (HUVEC) from damage by high ambient glucose. METHODS: HUVEC was incubated in glucose, 5 or 30 mmol/L, either alone or in the presence of morroniside (final concentration 100, 10, and 1 μmol/L, respectively) for 48 h. The proliferation of HUVEC was quantified by MTT method; its cycle was analyzed by flow cytometry; morphological change was observed with fluorescence microscopy. RESULTS: Survival of HUVEC cultured in high ambient glucose was significantly decreased when compared to that in normal concentration of glucose (Pcells entering into S-phase, along with severe morphological damage. With the intervention of morroniside (final concentration 100 and 10 μmol/L), the cell survival was significantly recovered (P<0.01, P<0.05, respectively), accompanied with increased S-phase rate and less extent of morphological damage. CONCLUSION: Morroniside protected HUVEC against high ambi- ent glucose induced injury, which suggested that morroniside could exert a beneficial effect on preventing diabetic angiopathies.

关键词： morroniside umbilical veins endothelial cells diabetic angiopathies