Hepatic sinusoidal endothelial cell(LSECs),as the sinusoidal capillary channel of the liver,is the most abundant non-parenchymal cell group in the liver. LSECs not only forms a barrier in the hepatic sinusoid,but also...Hepatic sinusoidal endothelial cell(LSECs),as the sinusoidal capillary channel of the liver,is the most abundant non-parenchymal cell group in the liver. LSECs not only forms a barrier in the hepatic sinusoid,but also has important physiological and immunological functions,including filtration,endocytosis,antigen presentation and leukocyte recruitment. It has been clear that LSECs play an important role in maintaining immune homeostasis in the liver and delaying the immune response to acute and chronic liver injury. In this review,we summarize how LSECs affect the immune microenvironment in the liver,and discuss their role in immune-mediated chronic liver disease,carcinogenesis,inflammation and aging process.展开更多
TNF-α is one of the most important proin-flammatory cytokines in mediating multiple physio-patho-logical functions during immunological responses. Vascular endothelial cells, when stimulated by TNF-α, can increase t...TNF-α is one of the most important proin-flammatory cytokines in mediating multiple physio-patho-logical functions during immunological responses. Vascular endothelial cells, when stimulated by TNF-α, can increase the expression of multiple cytokines and cellular adhesion molecules and, in turn, actively promote the inflammatory responses by recruiting and activating of leukocytes to the inflammatory site. In addition to endothelial death induced by TNF-α, we found for the first time that TNF-α can also induce the human endothelial cells senescence. The induced senescent endothelial cells will display SA-B-Gal staining and they were arrested in G0-G1 phase. We found that △(?)m would always be up-regulated in response to TNF-α stimula-tion at early time but when the cells become senescent, △(?)m shows a tendency to decrease. It may reflect the sthenic func-tion of mitochondria at early time in response to TNF-α stimulation and decay when the endothelial cells were in-duced senescent. ROS展开更多
目的:探讨炎症因子白介素-1α(interleukin-1α,IL-1α)对人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)衰老的影响,并探讨高迁移率族蛋白B1(high mobility group protein B1,HMGB1)在其中的作用及机制。方法:将HUV...目的:探讨炎症因子白介素-1α(interleukin-1α,IL-1α)对人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)衰老的影响,并探讨高迁移率族蛋白B1(high mobility group protein B1,HMGB1)在其中的作用及机制。方法:将HUVECs随机分为对照组(不加处理)、IL-1α组(10 ng/m L IL-1α孵育)、HMGB1组(100 ng/m L HMGB1孵育)、HMGB1+IL-1α组(100 ng/m L HMGB1和10 ng/m L IL-1α共同孵育),采用细胞衰老相关β-半乳糖苷酶(senescence associatedβ-galactosidase,SAβ-gal)染色检测细胞衰老数目,采用Western印迹检测沉默信息调节子1(silent information regulator 1,SIRT1)的蛋白表达,采用实时荧光定量PCR(quantitative real-time PCR,q RT-PCR)检测衰老相关基因p53,p21和p16的m RNA表达。结果:与对照组相比,IL-1α组SAβ-gal染色阳性细胞数目明显增加(P<0.05),SIRT1蛋白表达水平明显下调(P<0.01)。与IL-1α组相比,HMGB1+IL-1α组SAβ-gal染色阳性细胞减少,p21和p53的m RNA表达下调(均P<0.05),但p16的m RNA表达差异无统计学意义(P>0.05)。结论:IL-1α能诱导血管内皮细胞的衰老,其中HMGB1可能通过p53-p21途径抑制IL-1α诱导的内皮细胞衰老过程。展开更多
基金National Natural Science Foundation of China(No.81760151)。
文摘Hepatic sinusoidal endothelial cell(LSECs),as the sinusoidal capillary channel of the liver,is the most abundant non-parenchymal cell group in the liver. LSECs not only forms a barrier in the hepatic sinusoid,but also has important physiological and immunological functions,including filtration,endocytosis,antigen presentation and leukocyte recruitment. It has been clear that LSECs play an important role in maintaining immune homeostasis in the liver and delaying the immune response to acute and chronic liver injury. In this review,we summarize how LSECs affect the immune microenvironment in the liver,and discuss their role in immune-mediated chronic liver disease,carcinogenesis,inflammation and aging process.
文摘TNF-α is one of the most important proin-flammatory cytokines in mediating multiple physio-patho-logical functions during immunological responses. Vascular endothelial cells, when stimulated by TNF-α, can increase the expression of multiple cytokines and cellular adhesion molecules and, in turn, actively promote the inflammatory responses by recruiting and activating of leukocytes to the inflammatory site. In addition to endothelial death induced by TNF-α, we found for the first time that TNF-α can also induce the human endothelial cells senescence. The induced senescent endothelial cells will display SA-B-Gal staining and they were arrested in G0-G1 phase. We found that △(?)m would always be up-regulated in response to TNF-α stimula-tion at early time but when the cells become senescent, △(?)m shows a tendency to decrease. It may reflect the sthenic func-tion of mitochondria at early time in response to TNF-α stimulation and decay when the endothelial cells were in-duced senescent. ROS
文摘目的:探讨炎症因子白介素-1α(interleukin-1α,IL-1α)对人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)衰老的影响,并探讨高迁移率族蛋白B1(high mobility group protein B1,HMGB1)在其中的作用及机制。方法:将HUVECs随机分为对照组(不加处理)、IL-1α组(10 ng/m L IL-1α孵育)、HMGB1组(100 ng/m L HMGB1孵育)、HMGB1+IL-1α组(100 ng/m L HMGB1和10 ng/m L IL-1α共同孵育),采用细胞衰老相关β-半乳糖苷酶(senescence associatedβ-galactosidase,SAβ-gal)染色检测细胞衰老数目,采用Western印迹检测沉默信息调节子1(silent information regulator 1,SIRT1)的蛋白表达,采用实时荧光定量PCR(quantitative real-time PCR,q RT-PCR)检测衰老相关基因p53,p21和p16的m RNA表达。结果:与对照组相比,IL-1α组SAβ-gal染色阳性细胞数目明显增加(P<0.05),SIRT1蛋白表达水平明显下调(P<0.01)。与IL-1α组相比,HMGB1+IL-1α组SAβ-gal染色阳性细胞减少,p21和p53的m RNA表达下调(均P<0.05),但p16的m RNA表达差异无统计学意义(P>0.05)。结论:IL-1α能诱导血管内皮细胞的衰老,其中HMGB1可能通过p53-p21途径抑制IL-1α诱导的内皮细胞衰老过程。
