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Thinking outside the black box:are the brain endothelial cells the new main target in Alzheimer's disease? 被引量:2
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作者 Enrique Estudillo Adolfo López-Ornelas +3 位作者 Alejandro Rodríguez-Oviedo Neptali Gutiérrez de la Cruz Marco Antonio Vargas-Hernández Adriana Jiménez 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第12期2592-2598,共7页
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 molec... 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. 展开更多
关键词 DEMENTIA endothelial cells NEURODEGENERATION NEUROINFLAMMATION neuronal death paracellular transport transcellular transport
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降血压肽Val-Leu-Pro-Val-Pro在Caco-2细胞模型中的吸收机制 被引量:5
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作者 刘冬 孙海燕 +1 位作者 雷林 李世敏 《营养学报》 CAS CSCD 北大核心 2008年第4期354-358,362,共6页
目的研究降血压肽Val-Leu-Pro-Val-Pro(VLPVP)在Caco-2细胞模型中的吸收机制。方法用体外培养的Caco-2细胞单层模型,考察时间、pH值、药物浓度、吸收抑制剂及促进剂对VLPVP吸收的影响。用HPLC法检测VLPVP的浓度。结果VLPVP在pH7.4时转... 目的研究降血压肽Val-Leu-Pro-Val-Pro(VLPVP)在Caco-2细胞模型中的吸收机制。方法用体外培养的Caco-2细胞单层模型,考察时间、pH值、药物浓度、吸收抑制剂及促进剂对VLPVP吸收的影响。用HPLC法检测VLPVP的浓度。结果VLPVP在pH7.4时转运量最大,且与浓度和时间呈正相关。肽转运载体竞争性抑制剂Gly-Pro、arphamenine A和细胞内吞抑制剂氧化苯胂对VLPVP的转运没有显著的抑制作用,而旁路转运促进剂去氧胆酸钠、多药耐药蛋白抑制剂MK-571和能量抑制剂叠氮化钠对VLPVP从AP侧至BL侧的转运有非常显著的促进作用,而叠氮化钠和MK-571对VLPVP从BL侧至AP侧的转运无显著影响。结论VLPVP以旁路转运为主要方式被小肠上皮细胞吸收,并受到多药耐药蛋白MRP2强烈的外排作用。 展开更多
关键词 降血压肽 VaI-Leu-Pro-VaI-Pro CACO-2细胞 旁路转运 外排作用
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Defective claudin-10 causes a novel variation of HELIX syndrome through compromised tight junction strand assembly
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作者 Sebastian Sewerin Jorg Piontek +6 位作者 Ria Schonauer Sonja Grunewald Angelika Rauch Steffen Neuber Carsten Bergmann Dorothee Gunzel Jan Halbritte 《Genes & Diseases》 SCIE 2022年第5期1301-1314,共14页
Formation of claudin-10 based tight junctions(TJs)is paramount to paracellular Na+transport in multiple epithelia.Sequence variants in CLDN10 have been linked to HELIX syndrome,a salt-losing tubulopathy with altered h... Formation of claudin-10 based tight junctions(TJs)is paramount to paracellular Na+transport in multiple epithelia.Sequence variants in CLDN10 have been linked to HELIX syndrome,a salt-losing tubulopathy with altered handling of divalent cations accompanied by dysfunctional salivary,sweat,and lacrimal glands.Here,we investigate molecular basis and phenotypic consequences of a newly identified homozygous CLDN10 variant that translates into a single amino acid substitution within the fourth transmembrane helix of claudin-10.In addition to hypohidrosis(H),electrolyte(E)imbalance with impaired urine concentrating ability,and hypolacrimia(L),phenotypic findings include altered salivary electrolyte composition and amelogenesis imperfecta but neither ichthyosis(I)nor xerostomia(X).Employing cellular TJ reconstitution assays,we demonstrate perturbation of cis-and trans-interactions between mutant claudin-10 proteins.Ultrastructures of reconstituted TJ strands show disturbed continuity and reduced abundance in the mutant case.Throughout,both major isoforms,claudin-10a and claudin-10b,are differentially affected with claudin-10b showing more severe molecular alterations.However,expression of the mutant in renal epithelial cells with endogenous TJs results in wild-type-like ion selectivity and conductivity,indicating that aberrant claudin-10 is generally capable of forming functional paracellular channels.Thus,mutant proteins prove pathogenic by compromising claudin-10 TJ strand assembly.Additional ex vivo investigations indicate their insertion into TJs to occur in a tissue-specific manner. 展开更多
关键词 Claudin-10 HELIX syndrome paracellular transport Salt-losing tubulopathy Tight junction
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细胞连接分子对上皮组织物质转运的调控机制 被引量:3
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作者 杨斐 杨艳红 +4 位作者 张馨月 吴慧娟 阳长媛 朴胜华 雷自立 《生物技术》 CAS 2019年第2期199-204,共6页
细胞连接分子对上皮组织物质转运有重要的调节作用,其分子机制有待总结归纳。上皮组织中多数细胞连接分子参与形成紧密连接、粘附连接、桥粒连接和间隙连接等连接结构,调控细胞间转运和跨细胞运输。构成紧密连接的Claudin蛋白通过栅栏... 细胞连接分子对上皮组织物质转运有重要的调节作用,其分子机制有待总结归纳。上皮组织中多数细胞连接分子参与形成紧密连接、粘附连接、桥粒连接和间隙连接等连接结构,调控细胞间转运和跨细胞运输。构成紧密连接的Claudin蛋白通过栅栏功能、受体功能和维持上皮细胞极性三种机制在调控上皮组织物质运输中起到至关重要的作用,其它细胞连接分子通过对紧密连接的调控间接影响物质运输。由于Claudin家族的各成员之间的功能代偿作用及转录后调控对Claudin蛋白的表达的重要性,给细胞连接研究造成一定局限,新的研究方法和技术有待发展。该文总结归纳出上皮细胞间连接分子调控物质转运的三种方式及当前应用于检测连接分子的生物技术,为基础和临床研究提供参考。 展开更多
关键词 细胞连接分子 上皮组织 细胞间转运 跨细胞运输 紧密连接
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