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TRIM14 promotes endothelial activation via activating NF-κB signaling pathway

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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

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

Increased expression of osteoprotegerin in vascular smooth muscle cells from spontaneously hypertensive rats

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Journal of Geriatric Cardiology 2004年第1期1卷 49-54页

作者： Yongshan MOU Tianhua LEI Luning ZHAO Xiaojun ZHU mingui fu Yuqing E CHEN Cardiovascular Research Institute Morehouse School of Medicine 720 Westview Drive SW Atlanta GA 30310 USA Cardiovascular Research Institute Peking University Health Science Center 38 Xue Yuan Road Beijing 100083 China

Background Osteoprotegerin (OPG) is a secreted protein of the tumor necrosis factor receptor family, which regulates bone mass by inhibiting osteoclast differentiation and activation. Although OPG is expressed ubiquitously and abundantly in many tissues and cell types including vascular cells, the role of OPG in other tissues is *** previous studies demonstrated that OPG was highly expressed in vascular smooth muscle cells (VSMC) and upregulated during vascular lesion formation. Methods and Results We documented, by Northern blot analysis,that the expression of OPG was more prevalent in the aorta and cultured VSMC from spontaneously hypertensive rats (SI-IR) compared to Wistar-Kyoto rats (WKY). In addition, we found that the expression of Angiotensin II (Ang II)type I receptor (AT1R) in SHR VSMC was at significantly increased levels than in WKY VSMC. furthermore, Ang II potently induced the expression of OPG in VSMC in a time- and dose-dependent manner through the AT1R signaling pathway. Conclusions OPG expression was substantially greater in SHR VSMC, suggesting that OPG may be an important determinant of vascular remodeling in SHR.

关键词： osteoprotegerin hypertension vascular smooth muscle cells gene expression

TRIM47 is a novel endothelial activation factor that aggravates lipopolysaccharide-induced acute lung injury in mice via K63-linked ubiquitination of TRAF2

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Signal Transduction and Targeted Therapy 2022年第6期7卷 2041-2052页

作者： Yisong Qian Ziwei Wang Hongru Lin Tianhua Lei Zhou Zhou Weilu Huang Xuehan Wu Li Zuo Jie Wu Yu Liu Ling-Fang Wang Xiao-Hui Guan Ke-Yu Deng mingui fu Hong-Bo Xin The National Engineering Research Center for Bioengineering Drugs and the Technologies Institute of Translational MedicineNanchang University1299 Xuefu RdHonggu District 330031 NanchangChina Department of Biomedical Science School of MedicineUniversity of Missouri Kansas City2411 Holmes StreetKansas CityMO 64108USA

Endothelial activation plays an essential role in the pathogenesis of sepsis-induced acute lung injury,however,the detailed regulatory mechanisms remain largely ***,we reported that TRIM47,an E3 ubiquitin ligase of the tripartite motifcontaining protein family,was highly expressed in vascular endothelial ***47-deficient mice were effectively resistant to lipopolysaccharide(LPS)-induced acute lung injury and death by attenuating pulmonary ***47 was upregulated during TNFα-induced endothelial activation in *** of TRIM47 in endothelial cells inhibited the transcription of multiple pro-inflammatory cytokines,reduced monocyte adhesion and the expression of adhesion molecules,and suppressed the secretion of IL-1βand IL-6 in endothelial *** contrast,overexpression of TRIM47 promoted inflammatory response and monocyte adhesion upon TNFα*** addition,TRIM47 was able to activate the NF-κB and MAPK signaling pathways during endothelial ***,our experiments revealed that TRIM47 resulted in endothelial activation by promoting the K63-linked ubiquitination of TRAF2,a key component of the TNFαsignaling *** together,our studies demonstrated that TRIM47 as a novel activator of endothelial cells,promoted LPS-induced pulmonary inflammation and acute lung injury through potentiating the K63-linked ubiquitination of TRAF2,which in turn activates NF-κB and MAPK signaling pathways to trigger an inflammatory response in endothelial cells.

关键词： ubiquitin acute inhibited

ROLE OF CALCINEURIN IN ANGIOTENSIN II- INDUCED CARDIAC MYOCYTE HYPERTROPHY OF RATS

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Chinese Medical Sciences Journal 2001年第1期16卷 1-4页

作者：符民桂张继峰许松庞永政刘乃奎唐朝枢 Institute of Cardiovascular Research First Hospital Beijing Medical University Beijing 100034. China

The present study investigated the role of calcineurin in angiotensin II(AngII)- induced cardiac myocyte hypertrophy of rats. Method. The primary cardiac myocytes were cultured under the standard conditions. The calcineurin activity in AngII- treated cardiomyocytes was tested by using PNPP;protein synethsis rate was assessed by 3H- leucine incorporation; atrial natriuretic factor(ANF) mRNA level was determined by Northern blot analysis. Cell viability was estimated by lactate dehydrogenase(LDH) levels in cultured medium and by dyed cell numbers. Result. After stimulation of 10,100 and 1 000nmol/L of AngII, calcineurin activities in the cardiomyocytes were increased by 13％ ,57％ (P Conclusion. During AngII- induced cardiac myocyte hypertrophy, calcineurin signal pathway is activated, and inhibition of the pathway can attenuate AngII- induced cardiac myocyte hypertrophy, which suggests that the calcineurin signal pathway may play an important role in AngII- induced myocardial hypertrophy of rats.

关键词： calcineurin angiotensin II cardiac hypertrophy signal transduction

Central role of myeloid MCPIP1 in protecting against LPSinduced inflammation and lung injury

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Signal Transduction and Targeted Therapy 2017年第1期2卷 18-32页

作者： Yong Li Xuan Huang Shengping Huang Hui He Tianhua Lei Fatma Saaoud Xiao-Qiang Yu Ari Melnick Anil Kumar Christopher J Papasian Daping Fan mingui fu Department of Biomedical Science and Shock/Trauma Research Center School of MedicineUniversity of Missouri-Kansas CityKansas CityMissouriMOUSA Institute of Translational Medicine Nanchang UniversityNanchangJiangxiP.R.China Department of Cell Biology and Anatomy University of South Carolina School of MedicineColumbiaSCUSA Division of Molecular Biology and Biochemistry School of Biological SciencesUniversity of Missouri-Kansas CityKansas CityMissouriMOUSA Division of Hematology and Medical Oncology Weill Cornell Medical CollegeNew YorkNYUSA Division of Pharmacology and Toxicology School of PharmacyUniversity of Missouri-Kansas CityKansas CityMissouriMOUSA

Although systemic inflammatory responses attributable to infection may lead to significant lung injury,the precise molecular mechanisms leading to lung damage are poorly understood and therapeutic options remain ***,we show that myeloid monocyte chemotactic protein-inducible protein 1(MCPIP1)plays a central role in protecting against LPS-induced inflammation and lung ***-specific MCPIP1 knockout mice developed spontaneous inflammatory syndromes,but at a late age compared to global MCPIP1 knockout ***,mice with a myeloid-specific deletion of MCPIP1 were extremely sensitive to LPS-induced lung injury due to overproduction of proinflammatory cytokines and *** identified C/EBPβand C/EBPδ,two critical transcriptional factors that drive cytokine production and lung injury,as targets of MCPIP1 *** administration caused MCPIP1 protein degradation in the *** inhibition of MALT1,a paracaspase that cleaves MCPIP1,by MI-2 selectively increased the MCPIP1 protein levels in macrophages and in the ***,administration of MI-2 protected mice from LPS-induced inflammation,lung injury and ***,these results indicate that myeloid MCPIP1 is central in controlling LPS-induced inflammation and lung *** inhibition of MALT1 protease activity may be a good strategy to treat inflammatory diseases by enhancing MCPIP1 expression in myeloid cells.

关键词： inflammation myeloid lung

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烙铁头蛇毒对体外血凝及纤溶的影响

蛇志 1996年第4期8卷 10-13页

作者：符民桂朱柳管锦霞余清声广州医学院广州蛇毒研究所

行体外血凝及纤溶观察结果表明：①烙铁头蛇毒能明显延长凝血活酶时间（ＰＴＴ）、凝血酶原时间（ＰＴ）及蝰蛇毒磷脂时间（ＲＶＶＣＴ），显示出较强的抗凝活性；②对人纤维蛋白原及纤维蛋白有较强的溶解作用，这种作用不完全是单一的... 详细信息

行体外血凝及纤溶观察结果表明：①烙铁头蛇毒能明显延长凝血活酶时间（ＰＴＴ）、凝血酶原时间（ＰＴ）及蝰蛇毒磷脂时间（ＲＶＶＣＴ），显示出较强的抗凝活性；②对人纤维蛋白原及纤维蛋白有较强的溶解作用，这种作用不完全是单一的活化素样作用。

关键词：蛇毒烙铁头蛇毒血液凝固纤溶

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无接触电能传输技术的研究进展

电工技术学报 2010年第7期25卷 6-13页

作者：杨庆新陈海燕徐桂芝孙民贵傅为农天津工业大学电气工程与自动化学院天津300160 河北工业大学电气与自动化学院天津300130 匹兹堡大学医学中心宾夕法尼亚15260 香港理工大学电机系

无接触电能传输技术具有广泛的应用前景。目前主要的无接触电能传输方式有远场辐射、电磁共振和电磁感应直接耦合三种。远场辐射采取微波或激光来传递能量,频率最高,传输距离最远,效率也较低。电磁共振采用频率为MHz范围的谐振频率实现... 详细信息

无接触电能传输技术具有广泛的应用前景。目前主要的无接触电能传输方式有远场辐射、电磁共振和电磁感应直接耦合三种。远场辐射采取微波或激光来传递能量,频率最高,传输距离最远,效率也较低。电磁共振采用频率为MHz范围的谐振频率实现电能在波长范围内的中等距离高效率传输。基于电磁感应原理的电能传输技术相对比较成熟,频率较低,传输距离相对很小,传输效率较高。本文主要分析了这三种电能传输方式的特点及国内外研究现状,给出了该技术的应用前景及存在问题,也展示了一些研究结果。

关键词：无接触电能传输感应耦合磁共振耦合辐射研究进展

深度目标检测与图像分类相结合的棉花发育期自动识别方法

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中国科技论文 2018年第20期13卷 2309-2316页

作者：毋立芳汪敏贵付亨简萌北京工业大学信息学部北京100124

提出了一种深度目标检测与图像分类相结合的棉花发育期自动识别方法,首先观察和分析棉花各个发育期图像存在的不同特征,然后通过基于深度学习的图像分类实现对棉花三真叶期、五真叶期和现蕾期的自动识别,并通过深度目标检测自动检测图... 详细信息

提出了一种深度目标检测与图像分类相结合的棉花发育期自动识别方法,首先观察和分析棉花各个发育期图像存在的不同特征,然后通过基于深度学习的图像分类实现对棉花三真叶期、五真叶期和现蕾期的自动识别,并通过深度目标检测自动检测图像中的花朵和棉絮,最后综合2种算法的结果,实现对棉花完整发育期的自动识别。将所提方法用新疆乌兰乌苏农业气象站提供的2016年部分观察数据进行训练,再用农业气象站提供的2016年的其他数据和2017年的全部数据集进行测试,算法对棉花发育期的识别准确率分别可达80.52%和75.48%,表明所提方法可为棉花作物远程观测提供一种可行的解决方案。

关键词：农业气象观测图像分类目标检测深度学习棉花发育期