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

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

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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

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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

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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

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Efficacy of Dangua Fang(丹瓜方) on Endothelial cells damaged by oxidative stress

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Journal of Traditional Chinese Medicine 2022年第6期42卷 900-907页

作者： HENG Xianpei LI Liang YANG Liuqin WANG Zhita Department of Endocrinology People's Hospital Affiliated to Fujian University of Traditional Chinese MedicineFuzhou 350004China

OBJECTIVE: To evaluate the protective effects of serum containing Dangua Fang( 丹瓜方) on vascular endothelium damaged by oxidative stress. METHODS: Five experiments were completed in this paper. In the first experiment, we found the most suitable serum containing Dangua Fang by comparing groups with different serum containing Dangua Fang. In the second experiments we analyzed Dangua Fang influencing endothelial cell viability and apoptosis and cell cycle. The third experiment on Dangua Fang intervention of mitochondrial respiratory chain. The fourth experiment on Dangua Fang intervention of mitochondrial membrane potential. And finally, on the fifth experiment we researched the mechanism of Dangua Fang improving mitochondrial function by comparing the Na~+-k~+-ATPase and peroxisome proliferator-activated receptor-gamma coactivator-1alpha(PGC-1α) in the Dangua group with the diazoxide group and Co Q+Vit C group. RESULTS: We compared the control group in the first experiments and the OD values in DZ1 group was the most significant in all intervening groups. The recipe of DZ1(5% serum containing Dangua Fang) was used in the following experiments. Compared with the control group, cell viability, cell cycle(G2 + S), cytochrome c oxidase(COX), R3 red/green, R2 red/green, R1 red/green decreased and apoptosis, succinate dehydrogenase(SDH), green(R2 + R3), Na+-k+-ATPase, PGC-1α increased in the model group. Compared with the model group, cell viability, G2+S, COX, R3 red/green, R2 red/green, R1 red/green raised and apoptosis, green(R2 + R3), Na-K-ATPase decreased in the Dangua group;G2 + S, R3 red/green, R2 red/green, R1 red/green raised and green(R2 + R3) decreased in the Co Q + Vit C group. Na-K-ATPase increased in the combined group(P Endothelial cells damaged by promotion of mitochondrial biogenesis, reduction of Na~+-K~+-ATPase activity and regulation of mitochondrial respiratory chain function restoring mitochondrial membrane potential.

关键词： mitochondria oxidative stress Endothelial cells peroxisome proliferator-activated receptor gamma coactivator 1-alpha Dangua Fang

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The biological responses and mechanisms of Endothelial cells to magnesium alloy

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Regenerative Biomaterials 2021年第3期8卷 57-69页

作者： Zhe Hou Maolong Xiang Nuoya Chen Xiao Cai Bo Zhang Rifang Luo Li Yang Xiaoyi Ma Lifeng Zhou Fugui He Hongchi Yu Yunbing Wang National Engineering Research Center for Biomaterials Sichuan UniversityChengdu 610064China College of Life Sciences Sichuan UniversityChengdu 610064China The Fourth People’s Hospital of Chengdu Chengdu 610036China Beijing Key Laboratory of Cardiac Drug Device Technology and Evidence Based Medicine Beijing 100021China Institute of Biomedical Engineering West China School of Basic Medical Sciences&Forensic MedicineSichuan UniversityChengdu 610041China

Due to its good biocompatibility and degradability,magnesium alloy(Mg alloy)has shown great promise in cardiovascular stent applications.Rapid stent re-endothelialization is derived from migrated and adhered Endothelial cells(ECs),which is an effective way to reduce late thrombosis and inhibit hyperplasia.However,fundamental questions regarding Mg alloy affecting migration and adhesion of ECs are not fully understood.Here,we evaluated the effects of Mg alloy on the ECs proliferation,adhesion and migration.A global gene expression profiling of ECs co-culturing with Mg alloy was conducted,and the adhesion-and migration-related genes were examined.We found that Mg alloy had no adverse effects on ECs viability but significantly affected ECs migration and adhesion.Co-cultured with Mg alloy extract,ECs showed contractive adhesion morphology and decreased motility,which was supported by the down-regulation of adhesion-related genes(Paxillin and Vinculin)and migration-related genes(RAC 1,Rho A and CDC 42).Accordingly,the re-endothelialization of Mg alloy stent was inhibited in vivo.Our results may provide new inspiration for improving the broad application of Mg alloy stents.

关键词： magnesium alloy Endothelial cells migration adhesion

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Substrate stiffness differentially impacts autophagy of Endothelial cells and smooth muscle cells

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Bioactive Materials 2021年第5期6卷 1413-1422页

作者： Mi Hu Fan Jia Wei-Pin Huang Xu Li Deng-Feng Hu Jing Wang Ke-Feng Ren Guo-Sheng Fu Yun-Bing Wang Jian Ji MOE Key Laboratory of Macromolecular Synthesis and Functionalization Department of Polymer Science and EngineeringZhejiang UniversityHangzhou310027China Key Laboratory of Cardiovascular Intervention and Regenerative Medicine of Zhejiang Province Department of CardiologySir Run Run Shaw HospitalZhejiang UniversityHangzhou310016China National Engineering Research Center for Biomaterials Sichuan UniversityChengdu610064China

Stiffening of blood vessels is one of the most important characteristics in the process of many cardiovascular pathologies such as atherosclerosis,angiosteosis,and vascular aging.Increased stiffness of the vascular extracellular matrix drives artery pathology and alters phenotypes of vascular cell.Understanding how substrate stiffness impacts vascular cell behaviors is of great importance to the biomaterial design in tissue engineering,regenerative medicine,and medical devices.Here we report that changing substrate stiffness has a significant impact on the autophagy of vascular Endothelial cells(VECs)and smooth muscle cells(VSMCs).Interestingly,our findings demonstrate that,with the increase of substrate stiffness,the autophagy level of VECs and VSMCs showed differential changes:endothelial autophagy levels reduced,leading to the reductions in a range of gene expression associated with endothelial function;while,autophagy levels of VSMCs increased,showing a transition from contractile to the synthetic phenotype.We further demonstrate that,by inhibiting cell autophagy,the expressions of endothelial functional gene were further reduced and the expression of VSMC calponin increased,suggesting an important role of autophagy in response of the cells to the challenge of microenvironment stiffness changing.Although the underlying mechanism requires further study,this work highlights the relationship of substrate stiffness,autophagy,and vascular cell behaviors,and enlightening the design principles of surface stiffness of biomaterials in cardiovascular practical applications.

关键词： Substrate stiffness Autophagy Endothelial cells Smooth muscle cells Polyelectrolyte film

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Inhibitory Effects of Simvastatin on Oxidized Low-Density Lipoprotein-lnduced Endoplasmic Reticulum Stress and Apoptosis in Vascular Endothelial cells

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Chinese Medical Journal 2018年第8期131卷 950-955页

作者： Guo-Qiang Zhang Yong-Kang Tao Yong-Ping Bai Sheng-Tao Yan Shui-Ping Zhao Department of Emergency China-Japan Friendship Hospital Beijing 100029 China Department of Geriatric Medicine Xiangya Hospital Central South University Changsha Hunan 410008 China Department of Cardiology The Second Xiangya Hospital Central South University Changsha Hunan 410011 China

Background：Oxidized low-density lipoprotein （ox-LDL）-induced oxidative stress and endothelial apoptosis are essential for atherosclerosis. Our previous study has shown that ox-LDL-induced apoptosis is mediated by the protein kinase RNA-like endoplasmic reticulum kinase （PERK）/eukaryotic translation initiation factor 2α-subunit （eIF2α）/CCAAT/enhancer-binding protein homologous protein （CHOP） endoplasmic reticulum （ER） stress pathway in Endothelial cells. Statins are cholesterol-lowering drugs that exert pleiotropic effects including suppression of oxidative stress. This study aimed to explore the roles of simvastatin on ox-LDL-induced ER stress and apoptosis in Endothelial cells.Methods：Human umbilical vein Endothelial cells （HUVECs） were treated with simvastatin （0.1, 0.5, or 2.5 μmol/L） or DEVD-CHO （selective inhibitor of caspase-3, 100 μmol/L） for 1 h before the addition of ox-LDL （100 μg/ml） and then incubated for 24 h, and untreated cells were used as a control group. Apoptosis, expression of PERK, phosphorylation of eIF2α, CHOP mRNA level, and caspase-3 activity were measured. Comparisons among multiple groups were performed with one-way analysis of variance （ANOVA） followed by post hoc pairwise comparisons using Tukey’s tests. A value of P 〈 0.05 was considered statistically significant.Results：Exposure of HUVECs to ox-LDL resulted in a significant increase in apoptosis （31.9% vs. 4.9%, P 〈 0.05）. Simvastatin （0.1, 0.5, and 2.5 μmol/L） led to a suppression of ox-LDL-induced apoptosis （28.0%, 24.7%, and 13.8%, F = 15.039, all P 〈 0.05, compared with control group）. Ox-LDL significantly increased the expression of PERK （499.5%, P 〈 0.05） and phosphorylation of eIF2α （451.6%, P 〈 0.05）, if both of which in the control groups were considered as 100%. Simvastatin treatment （0.1, 0.5, and 2.5 μmol/L） blunted ox-LDL-induced expression of PERK （407.8%, 339.1%, and 187.5%, F = 10.121, all P 〈 0.05, compared with control group） and phosphorylation of eIF2α （407.8%, 339.1%, 187.5%, F = 11.430, all P 〈 0.05, compared w

关键词： Apoptosis Endoplasmic Reticulum Stress Endothelial cells Oxidized Low-Density Lipoprotein Simvastatin

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Down-regulation of miR-155 inhibits inflammatory response in human pulmonary microvascular Endothelial cells infected with influenza A virus by targeting sphingosine-1-phosphate receptor 1

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Chinese Medical Journal 2020年第20期133卷 2429-2436页

作者： Si-Mei Shen Hao Jiang Jiang-Nan Zhao Yi Shi Department of Respiratory and Critical Care Medicine Jinling HospitalMedical School of Nanjing UniversityNanjingJiangsu 210016China Department of Emergency Medicine The Second Affiliated HospitalSoutheast UniversityNanjingJiangsu 210003China

Background:Endothelial cells play a key role in the cytokine storm caused by influenza A virus. MicroRNA-155 (miR-155) is an important regulator in inflammation. Its role in the inflammatory response to influenza A infection, however, has yet to be elucidated. In this study, we explored the role as well as the underlying mechanism of miR-155 in the cytokine production in influenza A-infected Endothelial cells.Methods:Human pulmonary microvascular Endothelial cells (HPMECs) were infected with the influenza A virus strain H1N1. The efficiency of H1N1 infection was confirmed by immunofluorescence. The expression levels of proinflammatory cytokines and miR-155 were determined using real-time polymerase chain reaction. A dual-luciferase reporter assay characterized the interaction between miR-155 and sphingosine-1-phosphate receptor 1 (S1PR1). Changes in the target protein levels were determined using Western blot analysis.Results:MiR-155 was elevated in response to the H1N1 infection in HPMECs (24 h post-infection vs. 0 h post-infection, 3.875 ± 0.062 vs. 1.043 ± 0.013, P = 0.001). Over-expression of miR-155 enhanced inflammatory cytokine production (miR-155 mimic vs. negative control, all P < 0.05 in regard of cytokine levels) and activation of nuclear factor kappa B in infected HPMECs (miR-155 mimic vs. negative control, P = 0.004), and down-regulation of miR-155 had the opposite effect. In addition, S1PR1 was a direct target of miR-155 in the HPMECs. Inhibition of miR-155 enhanced the expression of the S1PR1 protein. Down-regulation of S1PR1 decreased the inhibitory effect of the miR-155 blockade on H1N1-induced cytokine production and nuclear factor kappa B activation in HPMECs. Conclusion:MiR-155 maybe modulate influenza A-induced inflammatory response by targeting S1PR1.

关键词： MicroRNA-155 Sphingosine 1-phosphate receptor 1 Influenza A virus Endothelial cells

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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

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