Feiyue Xing

Jinan University

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Pu Xiao

Shanghai Institute of Ceramics

Jia Xiao

Qingdao University

George L. Tipoe

University of Hong Kong

Haiwang Lai

Dongguan University of Technology

Jingfang Di

Jinan University

Boning Zeng

Jinan University

Kwok‐Fai So

University of Hong Kong

Jing Liu

Jinan University

Yingxia Liu

Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital

Yili Yang

Jinan University

Cooperative Institutions

Jinan University

Chinese Academy of Sciences

Sun Yat-sen University

University of Hong Kong

Peking University

First Affiliated Hospital of Jinan University

Southern Medical University

Sichuan University

Chinese Academy of Medical Sciences & Peking Union Medical College

Chinese University of Hong Kong

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Polymer-coated calcium peroxide nanoparticles as an oxygen self-supplying platform for enhanced photodynamic therapy

European Polymer Journal (2022)

Shan Liu Haiwang Lai Feiyue Xing Pu Xiao

Peroxide

Phototoxicity

10.1016/j.eurpolymj.2022.111458

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Citations (8)

In Situ Generated Crude Trithiocarbonate for Visible Light‐Mediated RAFT Polymerization of Acrylates**

ChemistrySelect (2021)

Qizhi Yang Yili Yang Wenli Liu Wei Tian Feiyue Xing

Abstract Reversible addition‐fragmentation chain transfer (RAFT) radical polymerization holds great promise in the design and massive production of functional polymeric materials. However, its practical application was restricted by the scale‐up production of chain transfer agents, the insufficient oxygen tolerance, and its environmental impact. In this work, a trithiocarbonate (TTC)‐based RAFT agent ethyl 2‐(((butylthio)carbonothioyl)thio)propanoate was synthesized in situ using shelf‐stable RAFT precursors, i. e ., sodium n ‐butyl trithiocarbonate (TTCS) and ethyl 2‐bromopropionate (EBrP). The crude product was then directly used in RAFT polymerization of acrylates under the irradiation of LED at 405 nm. First‐order polymerization kinetics was evidenced by proton nuclear magnetic resonance and size exclusion chromatography analysis. The measured molecular weights were close to the theoretical values and the dispersities of poly( tert ‐butyl acrylate)s (P t BAs) are as low as 1.08, thanks to the light‐induced activation of the RAFT agent. Well‐defined P t BA is also obtained in the presence of air, due to the intrinsic catalytic behavior of TTC. The proposed method greatly simplifies the set‐up of RAFT polymerization without compromising its control for the polymerization. And it also contributes to reducing the cost and environmental impact of the RAFT polymerization, being promising for the industrialization of RAFT polymerization.

Chain transfer

Raft

Living polymerization

10.1002/slct.202103086

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Citations (1)

In vivo toxicological evaluation of Anisomycin

Toxicology Letters (2011)

Zhengle Tang Feiyue Xing Di Chen Yu Yu Chunyan Yu

Anisomycin

10.1016/j.toxlet.2011.10.001

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Citations (41)

Anisomycin suppresses Jurkat T cell growth by the cell cycle-regulating proteins

Pharmacological Reports (2013)

Chunyan Yu Feiyue Xing Zhengle Tang Christian Bronner Xijian Lu

Anisomycin

Jurkat cells

10.1016/s1734-1140(13)71019-3

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Citations (18)

LncRNA HANR Promotes Tumorigenesis and Increase of Chemoresistance in Hepatocellular Carcinoma

Cellular Physiology and Biochemistry (2017)

Jia Xiao Yi Lv Fujun Jin Yingxia Liu Yi Ma

Hepatocellular carcinoma (HCC) is the fifth most common cancer in the world and the third leading cause of cancer-related death. Critical roles for long non-coding RNAs (lncRNAs) have recently been demonstrated for a variety of cancers, including hepatocellular carcinoma. However, the effect and mechanism of lncRNAs in HCC tumorigenesis and chemoresistance have not been extensively characterized.In the current study, we have identified a HCC-expressed lncRNA termed as HANR (HCC associated long non-coding RNA). We identified HANR by microarray analysis and validated its up-regulated expression by quantitative PCR. RNA pull-down and pathway analyses were conducted to evaluate physical and functional interactions with HANR. In vivo experiments were performed to assess tumorigenesis and increase of chemoresistance. In addition, the HANR expression in HCC specimens was detected by FISH. Xenograft and orthotopic mice model was constructed to observe the effect of HANR on tumorigenesis and chemoresistance in vivo.HANR was demonstrated to be up-regulated in HCC patients and HCC cell lines. Increased HANR expression in HCC predicted short survival of patients. Knock-down of HANR markedly retarded cell proliferation, suppressed HCC xenograft/orthotopic tumor growth, induced apoptosis and enhanced chemosensitivity to doxorubicin, while over-expression of HANR showed the opposite effects. It was found that HANR bind to GSKIP for regulating the phosphorylation of GSK3β in HCC.Our results demonstrate that HANR contributes to the development of HCC and is a promising therapeutic target for chemosensitization of HCC cells to doxorubicin, which may represent a promising therapeutic target in the future.

Liver Cancer

10.1159/000484116

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Citations (93)

[An infrared imaging system for detecting electrophoretic mobility shift of DNA-protein complexes].

PubMed (2009)

Yifei Wang Dehong Cai Hong Chen Yongyan Mo Na Yi

To establish a new non-radioactive method for electrophoretic mobility shift assay (EMSA) to investigate the binding between glucocorticoid induced leucine zipper (GILZ) and peroxisome proliferator-activated receptor-gamma 2 (PPARgamma2) promoter oligonucleotides.GILZ protein prepared by prokaryotic expression was linked to PPARgamma2 promoter oligonucleotides end-labeled with IRDye 800 infrared dye. The DNA-protein complex was separated with non-denatured polyacrylamide gel and scanned with the Odyssey. Infrared Imaging System.One lane of DNA-protein complex was clearly presented, and the signal intensity increased along with the increment of the protein load.This infrared imaging system can be used for EMSA for detecting the DNA-protein complex with high sensitivity efficiency and allows easy operation.

Polyacrylamide

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Antioxidant treatment enhances human mesenchymal stem cell anti-stress ability and therapeutic efficacy in an acute liver failure model

Scientific Reports (2015)

Wen Zeng Jia Xiao Zheng Gang Feiyue Xing George L. Tipoe

One of the major problems influencing the therapeutic efficacy of stem cell therapy is the poor cell survival following transplantation. This is partly attributed to insufficient resistance of transplanted stem cells to oxidative and inflammatory stresses at the injured sites. In the current study, we demonstrated the pivotal role of antioxidant levels in human umbilical cord mesenchymal stem cells (hUCMSCs) dynamic in vitro anti-stress abilities against lipopolysaccharide (LPS)/H2O2 intoxication and in vivo therapeutic efficacy in a murine acute liver failure model induced by D-galactosamine/LPS (Gal/LPS) by either reducing the antioxidant levels with diethyl maleate (DEM) or increasing antioxidant levels with edaravone. Both the anti- and pro-oxidant treatments dramatically influenced the survival, apoptosis, and reactive oxygen species (ROS) production of hUCMSCs through the MAPK-PKC-Nrf2 pathway in vitro. When compared with untreated and DEM-treated cells, edaravone-treated hUCMSCs rescued NOD/SCID mice from Gal/LPS-induced death, significantly improved hepatic functions and promoted host liver regeneration. These effects were probably from increased stem cell homing, promoted proliferation, decreased apoptosis and enhanced secretion of hepatocyte growth factor (HGF) under hepatic stress environment. In conclusion, elevating levels of antioxidants in hUCMSCs with edaravone can significantly influence their hepatic tissue repair capacity.

Cell therapy

Stem Cell Therapy

10.1038/srep11100

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Citations (83)

Effect of c-Jun N-terminal kinase on the proliferation of murine T lymphocytes

Zhonghua weishengwuxue he mianyixue zazhi (2007)

Zhe Yu Feiyue Xing Tong Wang Yaoying Zeng

目的研究c-Jun氨基末端激酶(c-Jun N-terminal kinase,JNK)在小鼠T细胞增殖中的作用.方法以活体染料羧基荧光素乙酰乙酸琥珀酰亚胺酯(CFSE)染色,建立了在多克隆刺激剂刀豆蛋白A(Con A)刺激下评价小鼠T细胞增殖的模型,通过流式细胞术分析JNK的一种新的特异性抑制剂SP600125存不同剂量、不同时间对T细胞增殖的影响,并应用CellQuest软件分析增殖细胞各代所占比例和增殖指数(PI)及抑制指数(HI).采用碘化丙锭染色分析不同剂量SP600125对Con A或佛波醇酯(PDB)加离子霉素(Ion)刺激的小鼠T细胞周期变化的作用.结果随着SP600125浓度从1.0μmol/L逐渐增至16.0 μmol/L,Con A对T细胞的促增殖作用逐渐减弱,以8.0～16.0 μmol/L的抑制作用最为明显,呈剂量依赖关系(r=0.98,P＜0.01);选择最佳剂量8.0 μmol/L,SP600125对T细胞增殖的抑制作用随时间从24 h递增至96 h而逐渐增强;进一步发现SP600125能使PDB加Ion刺激的小鼠T细胞停滞于G0/G1期,阻止其进入S期和G2/M期,且阻止作用随上述浓度的增加而增强,呈明显剂量依赖关系(S期:r=-0.98,P＜0.01;G2/M期:r=-0.88,P＜0.05);SP600125也呈剂量依赖性地使ConA诱导的T细胞停滞于F0/G1期,阻止其进入S期(r=-0.90,P＜0.05).结论 JNK信号通路的活化在小鼠T细胞增殖中可能起着重要作用。

c-jun

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Citations (1)

Jagged-1 signaling suppresses the IL-6 and TGF-β treatment-induced Th17 cell differentiation via the reduction of RORγt/IL-17A/IL-17F/IL-23a/IL-12rb1

Scientific Reports (2015)

Yuan Wang Feiyue Xing Siqi Ye Jia Xiao Jingfang Di

Abstract Jagged-1 signaling has recently been reported to be involved in the Th17 cell differentiation. However, little is known about its mechanisms. Soluble Jagged-1 was used to activate the Jagged-1–Notch signaling to interfere with the IL-6 and TGF-β-induced Th17 cell skewing. Genes relevant to the autoimmunity or inflammation were screened for the first time in this system by qPCR array for the differential expressions. The 18 genes out of 84, including Clec7a, Il12b, Il12rb1, Il12rb2, Csf3, Il15, Il17a, Il17f, Il17rc, Il17rd, Il17re, Il23a, Myd88, Socs1, Stat4, Stat5a, Sykb and Tbx21 , were downregulated, but only Cxcl2 , Cxcl12 and Mmp3 were upregulated. The expressions of the genes, Rorγt , Il17a , Il17f , Il12rb1 and Il23a , induced by simultaneous IL-6 and TGF-β treatment were significantly suppressed by Jagged-1, followed by the reduction of RORγt, IL-17A and IL-17F. Consistent with the attenuation of RORγt and the reduced production and secretion of IL-17A and IL-17F in the cell supernatant and the in situ stained cells, the number of CD4 + IL-17 + cells was also diminished. It is concluded that the Jagged-1–Notch signaling can suppress the IL-6 and TGF-β treatment-induced Th17 cell skewing through the attenuation of RORγt and, hence by, the down-regulation of IL-17A, IL-17F, IL-23a and IL-12rb1.

Interleukin-23

10.1038/srep08234

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Citations (27)

Deltex-1 is indispensible for the IL-6 and TGF-β treatment-triggered differentiation of Th17 cells

Cellular Immunology (2020)

Zhengle Tang Yuan Wang Rui Xing Shan Zeng Jingfang Di

CSL(CBF1, Su(H) and LAG-1)-dependent Hes-1 signaling plays an important part in regulating Th17 cell differentiation. However, little is known about influence of CSL-independent Deltex-1 signaling on this subset. The current focus is on roles of the Deltex-1 signaling in the Th17 cell differentiation. IL-17-producing CD4+ T cell subpopulation could be induced in vitro by treatment of both IL-6 and TGF-β. This could be reversed by knockdown of the deltex-1 gene, following the attenuation of retinoic acid-related orphan receptor γt (RORγt) and its DNA-binding activity in nuclei. Subsequently, Th17-associated cytokines generated by the treated cells were also diminished by the inhibition of Deltex-1 signaling, but the production of IL-10 was enhanced. Contrary to the alteration of RORγt, both zinc-finger transcription factor-3 (GATA3) and transcription factor Forkhead box P3 (Foxp3) were augmented at their mRNA and protein levels as well as DNA-binding activities with the emerging phenotypes of the corresponding cellular subpopulation and T-bet (encoded by TBX21) was not changed. These results reveal for the first time that Deltex-1 is indispensible for the IL-6 and TGF-β treatment-triggered differentiation of Th17 cells, indicating that CSL-independent Deltex-1 signaling favors naïve CD4+ T cells to deviate into Th17 cells via the enhancement of RORγt/IL-17A.

GATA3

10.1016/j.cellimm.2020.104176

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Citations (10)