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Puerarin@Chitosan composite for infected bone repair through mimicking the bio-functions of antimicrobial peptides

Bioactive Materials 2023年第3期21卷 520-530页

作者： Liping Ouyang Baohui Chen Xingdan Liu Donghui Wang Yang Li Yun Liao Kelvin W.K.Yeung Xuanyong Liu State Key Laboratory of High Performance Ceramics and Superfine Microstructure Shanghai Institute of CeramicsChinese Academy of SciencesShanghai200050China Hongqiao International Institute of edicine Shanghai Jiao Tong University School of MedicineShanghai200336China Cixi Center of Biomaterials Surface Engineering Ningbo315300China Department of Computational Biology for Individualised Medicine Centre for Individualised Infection Medicine(CiiM)&TWINCOREJoint Ventures Between the Helmholtz-Centre for Infection Research(HZI)and the Hannover Medical School(MHH)HannoverGermany Shenzhen Key Laboratory for Innovative Technology in Orthopaedic Trauma Guangdong Engineering Technology Research Center for Orthopaedic Trauma RepairDepartment of Orthopaedics and TraumatologyThe University of Hong Kong Shenzhen HospitalShenzhenChina

It is important to eliminate lipopolysaccharide(LPS)along with killing bacteria in periprosthetic joint infection(PJI)therapy for promoting bone repair due to its effect to regulate macrophages response.Although natural antimicrobial peptides(AMPs)offer a good solution,the unknown toxicity,high cost and exogenetic immune response hamper their applications in clinic.In this work,we fabricated a nanowire-like composite material,named P@C,by combining chitosan and puerarin via solid-phase reaction,which can finely mimic the bio-functions of AMPs.Chitosan,serving as the bacteria membrane puncture agent,and puerarin,serving as the LPS target agent,synergistically destroy the bacterial membrane structure and inhibit its recovery,thus endowing P@C with good antibacterial property.In addition,P@C possesses good osteoimmunomodulation due to its ability of LPS elimination and macrophage differentiation modulation.The in vivo results show that P@C can inhibit the LPS induced bone destruction in the Escherichia coli infected rat.P@C exhibits superior bone regeneration in Escherichia coli infected rat due to the comprehensive functions of its superior antibacterial property,and its ability of LPS elimination and immunomodulation.P@C can well mimic the functions of AMPs,which provides a novel and effective method for treating the PJI in clinic.

关键词： Osteoimmunomodulation Antibacterial Chitosan Puerarin Lipopolysaccharide

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Knockdown of long non-coding RNA LCPAT1 inhibits autophagy in lung cancer

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Cancer Biology & Medicine 2018年第3期15卷 228-237页

作者： Xiao Yu Xiaofei Ye Hongyan Lin Nannan Feng Sumeng Gao Xiaohong Zhang Yu Wang Herbert Yu Xiaobei Deng Biyun Qian hongqiao international institute of Medicine Shanghai Tongren Hospital and Faculty of Public Health Shanghai Jiao Tong University School of Medicine Cancer Epidemiology Program University of Hawaii Cancer Center

Objective: Long non-coding RNAs(lnc RNAs) are involved in numerous biological processes in lung cancer cells. In our previous studies, we identified a lnc RNA, ENST00000439577, which is highly expressed in lung carcinomas, and termed it lung cancer progression-associated transcript 1(LCPAT1). To characterize the role of LCPAT1 in lung cancer, we conducted the current study.Methods: Expression of LCPAT1 and autophagy-associated markers in tumor tissues and lung cancer cell lines was determined by real-time quantitative polymerase chain reaction(q PCR). Hematoxylin and eosin(HE) staining, q PCR, Western blot, and immunohistochemistry were performed to evaluate xenografted tumor tissues. Autophagy induced by rapamycin was detected by Western blot and immunofluorescence in lung cancer cell lines.Results: Expression of LCPAT1 and microtubule-associated protein 1 light chain 3 beta(LC3B) was positively correlated in lung cancer. Knockdown of LCPAT1 inhibited tumor growth and suppressed cell autophagy in vivo. Moreover, LCPAT1 knockdown in lung cancer cell lines resulted in decreased autophagy-associated gene expression and alleviated the cell autophagy induced by rapamycin.Conclusions: We speculate that LCPAT1 plays a crucial role in regulating autophagy in lung cancer.

关键词： RNA 非编码肺癌癌症 rapamycin 聚合酶链反应肿瘤生长生物过程

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Hematopoietic stem cell metabolism and stemness

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Blood Science 2019年第1期1卷 12-18页

作者： Dan Huang Chiqi Chen Li Xie Zhuo Yu Junke Zheng hongqiao international institute of Medicine Shanghai Tongren HospitalKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of EducationFaculty of Basic MedicineShanghai Jiao Tong University School of MedicineShanghaiChina

Hematopoietic stem cells(HSCs)are considered to originate from the aorta-gonad-mesonephros,migrate into fetal liver for a rapid expansion,and eventually reside into a unique hypoxic bone marrow niche,where they maintain their homeostasis throughout their life span.HSCs have been widely used for the treatment of many begin or malignant hematopoietic disorders.However,the unavailability of sufficient amount of HSCs still impedes their applications in the clinic.It is urgent to understand how HSC stemness or cell fates are determined at different developmental stages.Although many intrinsic and extrinsic factors(niche components)have been identified in the regulation of HSC origination,expansion,migration,and localization,the underlying mechanisms remain largely unknown.In this article,we summarize current views on the metabolic profiles of HSCs and related regulatory networks,which shows that intrinsic metabolic regulation may be critical for the cell fate determinations of HSCs:HSCs utilize glycolysis as their major energy sources;mitochondrial respiration is also required for the homeostasis of HSCs;amino acids,lipids,or other nutrient metabolisms also have unique roles in sustaining HSC activities.Mechanistically,many important regulatory pathways,such as MEIS1/HIF1A,MYC,PPM1K/CDC20,and ROS signals,are identified to fine-tune the nutrient metabolisms and cell fate commitments in HSCs.Nevertheless,more effort is required for the optimization or establishment of sensitive and specific metabolic techniques/systems for the metabolism studies in HSCs with limited cell numbers and exploring the metabolic profiles and fundamental regulatory mechanisms of different types of nutrients at each developmental stage of HSCs.

关键词： Bone marrow niche Glycolysis Hematopoietic stem cells Oxidative phosphorylation Stemness

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Ubiquitin-specific protease 47 regulates intestinal inflammation through deubiquitination of TRAF6 in epithelial cells

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Science China(Life Sciences) 2022年第8期65卷 1624-1635页

作者： Hu Lei Li Yang Hanzhang Xu Zhengting Wang Xiangyun Li Meng Liu Yingli Wu hongqiao international institute of Medicine Shanghai Tongren Hospital/Faculty of Basic MedicineKey Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of EducationShanghai Jiao Tong University School of MedicineShanghai 200025China Department of Gastroenterology Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China

Deubiquitinates(DUBs) alter the stabilities, localizations or activities of substrates by removing their ubiquitin conjugates,which are closely related to the development of inflammatory response. Here, we show that ubiquitin-specific protease 47(USP47) prevents inflammation development in inflammatory bowel disease(IBD). Compared with wild-type mice, Usp47 knockout mice are more susceptible to dextran sodium sulfate(DSS)-induced acute and chronic colitis with higher inflammatory cytokines expression and severe intestinal tissue damage. Chimeric mouse experiments suggest that non-hematopoietic cells mainly contribute to the phenotype. And, DSS-induced colitis of the Usp47 knockout mice depends on commensal bacteria.Mechanistically, down-regulation of USP47 aggravates the activation of NF-κB signaling pathway by increasing the K63-linked poly-ubiquitination of tumor necrosis factor receptor-associated factor 6(TRAF6) in intestinal epithelial cells. Furthermore, the expression of USP47, negatively correlated with the degree of inflammation, is lower at colonic inflammatory lesions than that non-inflammatory sites from the intestine from ulcerative colitis(UC) and Crohn's disease(CD) patients. These data, taken together, indicate that USP47 regulates intestinal inflammation through de-ubiquitination of K63-linked poly-ubiquitination TRAF6 in intestinal epithelial cells.

关键词： ubiquitin-specific protease 47 TRAF6 intestinal epithelial cell inflammation inflammatory bowel disease

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Promoter methylation of Wnt/β-Catenin signal inhibitor TMEM88 is associated with unfavorable prognosis of nonsmall cell lung cancer

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Cancer Biology & Medicine 2017年第4期14卷 377-386页

作者： Rongna Ma Nannan Feng Xiao Yu Hongyan Lin Xiaohong Zhang Oumin Shi Huan Zhang Shuo Zhang Lei Li Min Zheng Ming Gao Herbert Yu Biyun Qian hongqiao international institute of Medicine Shanghai Tongren Hospital/Faculty of Public HealthShanghai Jiao Tong University School of Medicine Key Laboratory of Cancer Prevention and Therapy Tianjin Medical University Cancer Institute and Hospital Cancer Epidemiology Program University of Hawaii Cancer Center

Objective:Recent research has indicated that altered promoter methylation of oncogenes and tumor suppressor genes is an important mechanism in lung cancer development and progression.In this study,we investigated the association between promoter methylation of TMEM88,a possible inhibitor of the Wnt/β-Catenin signaling,and the survival of patients with nonsmall cell lung cancer(NSCLC).Methods:Twelve pairs of tumor and adjacent non-tumor samples were used for microarray analyses of DNA methylation and gene expression.For validation,more than two hundred additional samples were analyzed for methylation using bisulfite pyrosequencing and for gene expression using q RT-PCR.Then the cell function were tested by wound healing,transwell,CCK8 and cell cycle assay.Results:Our analysis of patient specimens showed that TMEM88 methylation was higher in NSCLC tumors(82.2%±10.3,P56 months;P=0.021).In addition,we found that demethylation treatment could inhibit tumor cell proliferation,migration,and invasion,which was supportive of an association between methylation and survival.Conclusions:Based on these consistent observations,we concluded that TMEM88 may play an important role in NSCLC progression and that promoter methylation of TMEM88 may serve as a biomarker for NSCLC prognosis and treatment.

关键词： TMEM88 lung cancer methylation prognosis Wnt/β-Catenin signaling

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Localized surface plasmon resonance improves transdermal photodynamic therapy of hypertrophic scars

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Nano Research 2022年第5期15卷 4258-4265页

作者： Yunsheng Chen Zhixi Yu Xinxian Meng Hua Li Xiyang Sun Dannong He Yixin Zhang Zheng Zhang Department of Plastic and Reconstructive Surgery Shanghai Ninth People’s HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghai 200011China hongqiao international institute of Medicine Tongren HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghai 200336China Shanghai National Engineering Research Center for Nanotechnology Shanghai 200237China

Photodynamic therapy(PDT)is an emerging therapeutic strategy for hypertrophic scars(HS),which is heavily dependent on reactive oxygen species(ROS)generation.However,the unsatisfactory delivery and excitation of 5-aminolevulinic acid(ALA,a commercial photosensitizer in dermatology)result in an insufficient ROS generation,and thus limit the clinical application of PDT treating HS(HS-PDT).Consequently,sophisticated transdermal co-delivery nanoethosomes(named A/A-ES)with ALA and Au nanotriangles(AuNTs)in cores are prepared via an in-situ seed-mediated growth method,and then applied to improve HS-PDT through localized surface plasmon resonance(LSPR)-enhanced ROS generation.A/A-ES display a satisfactory performance in co-delivery in HS tissue with sufficient protoporphyrin IX production and LSPR effect in cytoplasm,which is beneficial for ALA excitation as well as ROS generation.In vitrolvivo studies reveal that A/A-ES significantly improve HS-PDT in promoting to fibroblast apoptosis and collagen remodeling through LSPR-enhanced ROS generation.Therefore,this study provides a feasible strategy that integrates transdermal delivery and LSPR to enable the beneficial effects of HS-PDT through boosting the delivery and excitation of ALA.

关键词： hypertrophic scars localized surface plasmon resonance nanoethosomes photodynamic therapy reactive oxygen species transdermal co-delivery

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Exploring the Advantages and Disadvantages of the China-Pakistan Free Trade Agreement

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China & World Economy 2021年第3期29卷 83-103页

作者： Mirajul Haq Javeria Saeed Muhammad Akram international institute of Islamic Economics(HIE) International Islamic University IslamabadPakistan international institute of Islamic Economics(HIE) International Islamic University Islamabad

This paper explores whether the China-Pakistan Free Trade Agreement(FTA),which entered into ejfect in 2007,has led to advantages or disadvantages for the participating countries.It assesses the gains and losses associated with the agreement rigorously using two different approaches.First,the revealed comparative advantage index is calculated for 10 commodity groups.This identifies the commodity groups in which the participating countries have a comparative advantage.Second,trade creation and trade diversion are estimated for overall imports and for the commodity-group level imports.This analysis provides useful information about the commodity groups in which a particular party to the FTA is experiencing an advantage or a disadvantage.The findings of the study show that China has an advantage in producing capital-intensive goods whereas Pakistan has a comparative advantage in the production of primary and semimanufactured goods.The empirical findings also indicate that,overall,the formation of the bilateral free trade agreement between Pakistan and China enhances trade with member countries as well as with nonparticipating countries.

关键词： gravity model panel data revealed comparative advantage trade creation trade diversion

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Comprehensive analysis of the expression and prognosis for APOE in malignancies: A pan-cancer analysis

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Oncology Research 2022年第1期30卷 13-22页

作者： SHOUKAI YU LINGMEI QIAN JUN MA hongqiao international institute of Medicine&Clinical Research Center Tongren HospitalShanghai Jiao Tong University School of MedicineShanghaiChina Clinical Research institute Shanghai Jiao Tong University School of MedicineShanghaiChina Harvard T.H.Chan School of Public Health Harvard UniversityBostonUSA

Apolipoprotein E(APOE),a gene identiﬁed as one of the strongest genetic factors contributing to the risk determinant of developing late-onset Alzheimer’s disease(AD),may also contribute to the risk of cancer.However,no pan-cancer analysis has been conducted speciﬁcally for the APOE gene.In this study,we investigated the oncogenic role of the APOE gene across cancers by GEO(Gene Expression Omnibus)and TCGA(The Cancer Genome Atlas).Based on the available data,we found that most cancer types overexpress APOE,and clear associations exist between the expression level of APOE and prognosis in tumor patients.The expression of APOE also correlates with certain gender-associated tumors including,ovarian cancer,uterine carcinosarcoma,and breast cancer.However,there is a signiﬁcant negative association between cancer-associatedﬁbroblast inﬁltration levels and the expression level of APOE in testicular germ cell tumors.Moreover,acute inﬂammatory response and protein-activation cascade-associated functions play an important role in the functional mechanisms of APOE.The present pan-cancer analysis of APOE shows that the protein phosphorylation,DNA methylation,and genetic alterations of APOE have a signiﬁcant clinical relevance for survival prognosis and immune cell inﬁltration.This novel pan-cancer study outlines the current understanding of APOE oncogenic roles across thirty-three cancers and highlights the complex association between AD and cancers.

关键词： APOE Pan-cancer Bioinformatics Alzheimer’s disease

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Brain-machine-brain interfaces as the foundation for the next generation of neuroprostheses

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National Science Review 2022年第10期9卷 8-10页

作者： Miguel A.L.Nicolelis Department of Neurobiology Duke University international institute of Neuroscience Edmond and Lily Safra

Back in 2011,my laboratory at the Duke University Center for Neuroengineering proposed a new variation on the already-classic paradigm known as brain-machine interfaces (BMIs)[1].In a series of experiments [2],we showed that monkeys could not only learn to employ electrical signals from large neuronal ensembles (300-700 neurons)located in the primary motor cortex(M1) to control the movements of an avatar arm and hand—i.***.using a typical BMI paradigm—but that they could also interpret in real time,streams of electrical signals delivered directly to their primary somatosensory cortex (S1) via cortical microstimulation.This strategy was created to allow these monkeys to perform a tactile discrimination task,without any interference from their physical bodies.Thus,instead of using their real finger tips to perform such a task,this approach allowed our monkeys to use their brain activity to directly control the movements of’virtual finger tips to scan the texture of a series of virtual objects.Upon receiving,via cortical microstimulation,electrical signals directly into their S1 that were proportional to the virtual surface textures of these objects,the monkeys learned to quickly select the correct object that they needed to identify to receive a reward.Essentially,

关键词： SPINAL-CORD STIMULATION

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Inhibitory leukocyte immunoglobulin-like receptors in cancer development

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Science China(Life Sciences) 2015年第12期58卷 1216-1225页

作者： ZHANG FeiFei ZHENG JunKe KANG XunLei DENG Mi LU ZhiGang KIM Jaehyup ZHANG ChengCheng hongqiao international institute of Medicine Shanghai Tongren Hospital Faculty of Basic Medicine Shanghai Jiao Tong University School of Medicine Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education Shanghai Jiao Tong University School of Medicine Departments of Physiology and Developmental Biology University of Texas Southwestern Medical Center

Inhibitory leukocyte immunoglobulin-like receptors(LILRB1-5) signal through immunoreceptor tyrosine-based inhibitory motifs(ITIMs) in their intracellular domains and recruit phosphatases protein tyrosine phosphatase, non-receptor type 6(PTPN6, SHP-1), protein tyrosine phosphatase, non-receptor type 6(PTPN6, SHP-2), or Src homology 2 domain containing inositol phosphatase(SHIP) to negatively regulate immune cell activation. These receptors are known to play important regulatory roles in immune and neuronal functions. Recent studies demonstrated that several of these receptors are expressed by cancer cells. Importantly, they may directly regulate development, drug resistance, and relapse of cancer, and the activity of cancer stem cells. Although counterintuitive, these findings are consistent with the generally immune-suppressive and thus tumor-promoting roles of the inhibitory receptors in the immune system. This review focuses on the ligands, expression pattern, signaling, and function of LILRB family in the context of cancer development. Because inhibition of the signaling of certain LILRBs directly blocks cancer growth and stimulates immunity that may suppress tumorigenesis, but does not disturb normal development, LILRB signaling pathways may represent ideal targets for treating hematological malignancies and perhaps other tumors.

关键词：免疫球蛋白受体表达肿瘤细胞白细胞蛋白酪氨酸磷酸酶信号转导免疫细胞调节作用

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