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TRIM14 promotes endothelial activation via activating NF-κB signaling pathway

Journal of Molecular Cell Biology 2020年第3期12卷 176-189页

作者： Xuan Huang Yong Li Xiuzhen Li Daping Fan Hong-Bo Xin Mingui Fu Institute of Translational Medicine Nanchang UniversityNanchang 330031China Department of Biomedical Science and Shock/Trauma Research Center School of MedicineUniversity of Missouri-Kansas CityKansas CityMO 64108USA Department of Cell Biology and Anatomy University of South Carolina School of MedicineColumbiaSC 29209USA

endothelial activation by proinflammatory cytokines is closely associated to the pathogenesis of atherosclerosis and other vascular diseases;however, the molecular mechanisms controlling endothelial activation are not fully understood. Here we identify TRIM14 as a new positive regulator of endothelial activation via activating NF-κB signal pathway. TRIM14 is highly expressed in human vascular endothelial cells (ECs) and markedly induced by inflammatory stimuli such as TNF-α, IL-1β, and LPS. Overexpression of TRIM14 significantly increased the expression of adhesion molecules such as VCAM-1, ICAM-1, E-selectin, and cytokines such as CCL2, IL-8, CXCL-1, and TNF-α in activated ECs and by which it facilitated monocyte adhesion to ECs. Conversely, knockdown of TRIM14 has opposite effect on endothelial activation. Upon TNF-α stimulation, TRIM14 is recruited to IKK complex via directly binding to NEMO and promotes the phosphorylation of IκBα and p65, which is dependent on its K63-linked ubiquitination. Meanwhile, p65 can directly bind to the promoter regions of human TRIM14 gene and control its mRNA transcription. Finally, TRIM14 protein level is significantly upregulated in mouse and human atheroma compared to normal arteries. Taken together, these results indicate that TRIM14-NF-κB forms a positive feedback loop to enhance EC activation and TRIM14 may be a potential therapeutic target for vascular inflammatory diseases such as atherosclerosis.

关键词： TRIM14 NF-κB endothelial activation atherosclerosis

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Intracellular endothelial Cell-derived Immunoglobulin Free Light Chain Induces endothelial activation through NF-κB Pathway

Intracellular Endothelial Cell-derived Immunoglobulin Free L...

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第十二届全国免疫学学术大会

作者： Jiang Dongyang Fan Linlin Xu Xu Yu Ze Qiu Xiaoyan Pang Jinjiang Tenth People's Hospital of Tongji University Peking University Dalian Medical University

Background:Immunoglobulin(Ig)plays an important role in humoral immune response by binding to antigens,as a secreted tetramer consisting of two identical heavy chains and two identical light ***,Ig free light chain(FL... 详细信息

关键词： Immunoglobulin Free Light Chain endothelial activation NF-κB

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TRIM65 E3 ligase targets VCAM-1 degradation to limit LPS-induced lung inflammation

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Journal of Molecular Cell Biology 2020年第3期12卷 190-201页

作者： Yong Li Xuan Huang Fang Guo Tianhua Lei Shitao Li Paula Monaghan-Nichols Zhisheng jiang Hong-Bo Xin Mingui Fu Department of Biomedical Science School of MedicineUniversity of Missouri-Kansas CityKansas CityMO 64108USA Institute of Translational Medicine Nanchang UniversityNanchang 330031China Institute of Cardiovascular Diseases Department of PathophysiologyHengyang Medical CollegeUniversity of South ChinaHengyang A21001China Department of Physiological Sciences Center for Veterinary and Health sciencesOklahoma State UniversityStillwaterOK 7A078USA

Although the adhesion molecules-mediated leukocyte adherence and infiltration into tissues is an important step of inflammation,the post-translational regulation of these proteins on the endothelial cells is poorly ***,we report that TRIM65,an ubiquitin E3 iigase of tripartite protein family,selectively targets vascular cell adhesion molecule 1(VCAM-1)and promotes its ubiq-uitination and degradation,by which it critically controls the duration and magnitude of sepsis-induced pulmonary ***65 is constitutively expressed in human vascular endothelial *** TNFa-induced endothelial activation,the protein levels ofTRIM65 and VCAM-1 are inversely *** of wild-type TRIM65,but not expression of aTRIM65 mutant that lacks E3 ubiquitin ligase function in endothelial cells,promotes VCAM-1 ubiquitination and degradation,whereas small interference RNA-mediated knockdown of TRIM65 attenuates VCAM-1 protein *** experiments show that TRIM65 directly interacts with VCAM-1 protein and directs its polyubiquitination,by which TRIM65 controls monocyte adherence and infiltration into tissues during ***,TRIM65-deficient mice are more sensitive to lipopolysaccharide-induced death,due to sustained and severe pulmonary *** together,our studies suggest that TRIM65-mediated degradation of VCAM-1 represents a potential mechanism that controls the duration and magnitude of infiammation.

关键词： TRIM65 VCAM-1 endothelial activation lung inflammation ubiquitination

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Functional nano-vector boost antiatherosclerosis efficacy of berberine in Apoe(-/-) mice

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Acta Pharmaceutica Sinica B 2020年第9期10卷 1769-1783页

作者： Xiaolei Ma Tingting Zhang Zhigang Luo Xiaolin Li Miao Lin Rui Li Peng Du Xiaoyou Yu Chen Ma Pengju Yan Jin Su Lulu Wang Yuhuan Li Jiandong Jiang State Key Laboratory of Bioactive Substance and Function of Natural Medicines Beijing City Key Laboratory of Drug Delivery Technology and Novel FormulationsInstitute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100050China Department of Pharmacy Jiamusi UniversityJiamusi 154007China Institute of Medicinal Biotechnology Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100050China

Atherosclerosis(AS)is the leading cause of heart attacks,stroke,and peripheral vascular ***(BBR),a botanical medicine,has diversified anti-atherosclerotic effects but with poor *** aim of this study was to develop an effective BBR-entrapped nano-system for treating AS in high-fat diet(HFD)-fed Apoe(-/-)mice,and also explore the possible underlying mechanisms *** D-a-tocopherol polyethylene glycol(PEG)succinate(TPGS)analogues with different PEG chain lengths were synthesized to formulate BBR-entrapped ***-fed Apoe(-/-)mice were administered with optimized formula(BBR,100 mg/kg/day)orally for 5 *** artery plaque onset and related metabolic disorders were evaluated,and the underlying mechanisms were *** data showed that,BT1500M increased BBR deposition in liver and adipose by 107.6%and 172.3%,*** the Apoe(-/-)mice,BT1500M ameliorated HFD-induced hyperlipidemia and lipid accumulation in liver and ***1500M also suppressed HFD-induced chronic inflammation as evidenced by the reduced liver and adipose levels of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β);and decreased plasma level of TNF-α,IL-6,IL-1β,interferon-γ(IFN-γ),monocyte chemotactic protein(MCP),and macrophage inflammatory factor(MIP).The mechanism study showed that BT1500M changed Ampk and Nf-Kb gene expression,and interrupted a crosstalk process between adipocytes and *** investigation proved that BT1500M decreased endothelial lesion and subsequent macrophage activation,cytokines release,as well as cholesteryl ester gathering in the aortic arch,resulting in ameliorated artery plaque *** results provide a practical strategy for treating AS using a BBR-entrapped nano-system.

关键词： Atherosclerosis Berberine Functional nano-vector endothelial activation

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