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Circular patterns of calcium oxalate crystals induced by defective Langmuir-Blodgett film

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Science China Chemistry 2008年第1期51卷 25-30页

作者： DENG SuiPing OUYANG JianMing XIE YuShan xing feiyue Institute of Biomineralization and Lithiasis Research Jinan UniversityGuangzhou 510632China

The injury of the renal epithelial cell membrane can promote the nucleation of nascent crystals, as well as adhesion of crystals on it. It thus accelerates the formation of renal calculi. In this paper, the defective Langmuir-Blodgett (LB) films were used as a model system to simulate the injured renal epithelial cell membrane. The microcosmic structure of the defective LB film and the molecular mechanism of the effect of this film on nucleation, growth, deposited patterns and adhesion of calcium oxalate monohydrate (COM) were investigated. The circular defective domains were formed in dipalmitoylphosphatidylcholine (DPPC) LB film after the film was treated by potassium oxalate. These domains could induce ring-shaped patterns of COM crystals. In comparison, the LB film without pretreatment by potassium oxalate only induced random growth of hexagonal COM crystals. As the crystallization time increased, the size of COM crystals in the patterns increased, the crystal patterns changed from empty circles to solid circles, and the number of the circular patterns with small size (5-20 μm) increased. The results would shed light on the molecular mechanism of urolithiasis induced by injury of the renal epithelial membrane at the molecular and supramolecular level.

关键词： defective LB Film calcium oxalate SEM biomineralization

Soluble Jagged 1/Fc chimera protein induces the differentiation and maturation of bone marrow-derived dendritic cells

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Chinese Science Bulletin 2008年第7期53卷 1040-1048页

作者： xing feiyue LIU Jing YU Zhe JI YuHua Institute of Tissue Transplantation and Immunology Department of Immunology Jinan University Guangzhou 510632 China Department of Stomatology Jinan University Guangzhou 510632 China

A soluble Jagged 1/Fc chimera protein (Jagged 1/Fc) was directly used to induce differentiation and maturation of bone marrow-derived dendritic cells (DCs) in mice in vitro. A model of inducing and am-plifying DCs in vitro was established. The effect of Jagged 1/Fc on morphology of DCs induced by both rmGM-CSF and rmIL-4 was observed under a confocal microscope. A fluorescein-labeled monoclonal antibody staining combined with flow cytometry was applied to detect the effect of Jagged 1/Fc on the expression of CD11c, MHC-II, CD86, CD80 and CD40 molecules on the surface of DCs. The results showed that Jagged 1/Fc did not affect the morphological properties of DC differentiation induced by both rmGM-CSF and rmIL-4. But it could promote the differentiation and maturation of DCs induced by both. The effect of it was strikingly different in the expression profile of co-stimulating molecules and the morphologic properties of DCs from lipopolysaccharide (LPS). The levels of MHC-II and CD40 molecule expression on the surface of DCs stimulated by Jagged 1/Fc were significantly lower than those stimulated by LPS, and the level of CD80 expression on the surface of DCs induced by Jagged 1/Fc was near to that induced by LPS. Jagged 1/Fc had no influence on the expression of CD86 mole-cule on the surface of DCs. Jagged 1/Fc when used alone could not maintain the growth, differentiation and maturation of DCs. All the findings indicate that Jagged 1/Fc influences the differentiation and maturation of DCs, which is not markedly similar to LPS, providing important evidence for its devel-opment and application as a novel immunosuppressant.

关键词：嵌合体蛋白质份化现象成熟现象骨质

A novel cell subset:Interferon-producing killer dendritic cells

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Science China(Life Sciences) 2008年第8期51卷 671-675页

作者： WANG JiongKun & xing feiyue Institute of Tissue Transplantation and Immunology, Jinan University, Guangzhou 510632, China Institute of Tissue Transplantation and Immunology Jinan University Guangzhou China

Recent reports introduce a novel cell subset of DCs with antigenic phenotypes shared by both NK cells and B cells, but without surface markers of pDCs and T cells, appearing to be a chimera of NK cells and DCs, namely interferon-producing killer dendritic cells(IKDCs).IKDCs not only secret type I and type II interferons to recognize and kill tumor cells effectively, but also express MHC-II molecules to present ***, IKDCs are considered as important immunosurveilance cells for tumors, providing a link between innate and adaptive immunity.

关键词： IKDCs cDCs pDCs NK cells

TPOL triggers apoptosis with mitochondrial injury through activating a ROS-dependent p53/p21/p27/Rb/Bax/Cyto C/caspase-mediated signaling

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中国病理生理杂志 2024年第8期40卷 1488-1496页

作者： CHENG Zongwei ZENG Boning xing feiyue Department of Immunobiology Institute of Tissue Transplantation and ImmunologyJinan UniversityGuangzhou 510632China

AIM:To explore the influence of ethyl(2,4,6-trimethylbenzoyl)phenylphosphinate(TPOL)on cell apoptosis and its potential ***:HEK293T cells sensitive to TPOL were treated with different concentrations of TPOL with or without exposure to light radiation,before treatment with various inhibitors,N-acetyl-Lcysteine(NAC),pifithrin-αand *** viability was measured by CCK-8 *** V/propidium iodide staining was used to count the number of apoptotic ***-DA staining was used to detect reactive oxygen species(ROS)levels,and JC-1 staining was used to assess mitochondrial membrane potential by flow *** expression of apoptosis-related proteins and cell cycle-regulated molecules was measured by Western ***:TPOL enhanced the apoptosis of HEK293T cells in a dose-dependent manner(P<0.05),with a decrease in Bcl-2 and increases in Bax and cytochrome C(Cyto C),followed by up-regulation of activated caspase-9 and caspase-3,and the cleavage of PARP(P<0.05).The TPOL-enhanced cleavage of caspase-3 and PARP was rescued by Z-DVED-FMK(P<0.01).TPOL also led to a rapid increase in ROS,a reduction in mitochondrial membrane potential,and the release of Cyto C(P<0.01),all of which could be reversed by the ROS scavenger ***,the TPOL-caused alterations in p21,p27,Rb,and CDK2 were also recovered by the p53 inhibitor pifithrin-α(P<0.05).The TPOL-induced changes in Bax,Bcl-2,cleaved caspase-9,activated caspase-3,and cleaved PARP were subsequently rescued by pretreatment with pifithrin-α(P<0.05).CONCLUSION:TPOL can induce cellular apoptosis with ROS-mediated mitochondrial membrane damage through the activation of a ROS-dependent p53/p21/p27/Rb/Bax/Cyto C/caspase-mediated signal axis.

关键词： ethyl(2,4,6-trimethylbenzoyl)phenylphosphinate reactive oxygen species mitochondria apoptosis

Garlic-derived compound S-allylmercaptocysteine inhibits hepatocarcinogenesis through targeting LRP6/Wnt pathway

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Acta Pharmaceutica Sinica B 2018年第4期8卷 575-586页

作者： Jia Xiao feiyue xing Yingxia Liu Yi Lv Xiaogang Wang Ming-Tat Ling Hao Gao Songying Ouyang Min Yang Jiang Zhu Yu Xia Kwok-Fai So George L.Tipoe State Key Discipline of Infectious Diseases Shenzhen Third People's Hospital Department of Immunobiology Institute of Tissue Transplantation and ImmunologyJinan University School of Biomedical Sciences The University of Hong Kong Department of Cell Biology & Institute of Biomedicine Jinan University Australian Prostate Cancer Research Centre-Queensland and Institute of Health and Biomedical Innovation Queensland University of Technology Institute of Traditional Chinese Medicine and Natural Products College of PharmacyJinan University Biomedical Research Center of South China College of Life SciencesFujian Normal University JM Medical (Shenzhen) LLC GMH Institute of Central Nervous System Regeneration Jinan University

Whether and how garlic-derived S-allylmercaptocysteine(SAMC) inhibits hepatocellular carcinoma(HCC) is largely unknown. In the current study, the role of low-density lipoprotein receptor(LDLR)-related protein 6(LRP6) in HCC progression and the anti-HCC mechanism of SAMC was examined in clinical sample, cell model and xenograft/orthotopic mouse models. We demonstrated that SAMC inhibited cell proliferation and tumorigenesis, while induced apoptosis of human HCC cells without influencing normal hepatocytes. SAMC directly interacted with Wnt-pathway co-receptor LRP6 on the cell membrane. LRP6 was frequently over-expressed in the tumor tissue of human HCC patients(66.7% of 48 patients) and its overexpression only correlated with the over-expression of β-catenin, but not with age, gender, tumor size, stage and metastasis. Deficiency or over-expression of LRP6 in hepatoma cells could partly mimic or counteract the anti-tumor properties of SAMC, respectively. In vivo administration of SAMC significantly suppressed the growth of Huh-7 xenograft/orthotopic HCC tumor without causing undesirable side effects. In addition, stable down-regulation of LRP6 in Huh-7 facilitated the anti-HCC effects of SAMC. In conclusion, LRP6 can be a potential therapeutic target of HCC. SAMC is a promising specific anti-tumor agent for treating HCC subtypes with Wnt activation at the hepatoma cell surface.

关键词： S-allylmercaptocysteine HCC Wnt LRP6 Human Nude mice

ICBP90 mediates Notch signalling to promote human hepatocellular carcinoma growth

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ICBP90 mediates Notch signalling to promote human hepatocell...

第十届全国免疫学学术大会

作者： Haifeng Fu Yuting Li Jia Xiao Pengtao You Jing Liu feiyue xing Institute of Tissue Transplantation and Immunology Department of Immunobiology Jinan University

Notch signaling pathway plays a key role in cell proliferation and *** are also closely related to an inverted CCAAT box binding protein(ICBP90).But little is known about whether there is correlation between Notch signaling and *** aim of the current study was to elucidate *** assay and flow cytometry were used to determine proliferation,cell cycle and apoptosis of hepatocellular carcinoma Hep G2 cells treated by N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester(DAPT).RT-PCR,Western Blot and in situ immuno-fluorescence staining were employed to examine expression of *** caused the inhibition of Notch signaling pathway activation,followed by the arrest of Hep G2 cell proliferation mainly at G0/G1,S and G2/M phases,and the enhancement of Hep G2cell ***90 and Hes-1 were highly expressed in the untreated Hep G2 *** reduction of NICD occurred in Hep G2 cells after the treatment of DAPT,followed by the down-regulation of ICBP90 with the increasing doses of *** knockdown of Hes-1 gene,that encodes a critical transcriptional factor in Notch pathway,also led to the similar alteration of *** could also result in the reduction of ICBP90,but the change of ICBP90 provokedby adriamycin was not accompanied with the alteration of ***90 was almost fully expressed in the nuclei,but Hes-1 was visible within both the cytoplasm and *** novel findings strongly indicate that Notch signalling promotes hepatocellular carcinoma progress through ICBP90 mediation.

关键词： ICBP90 Notch signal DAPT hepatocellular carcinoma growth

The preparation and characterization of novel TM-loaded selenium nanoparticle SeNPs@TM

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The preparation and characterization of novel TM-loaded sele...

广东省生物物理学会2013年学术研讨会

作者： Yu Xia Fangfang Xu Jia Xiao Jingfang Di Shan Zeng Jing liu feiyue xing Department of immunobiology Institute of tissue transplantation and immunologyJinan University

Introduction Selenium nanomaterials and related materials have attracted increased attention for their unique charact-eristics and potential applications in biological *** recent years, considerable studies have focused on the preparation of elemental selenium(Se) *** as an essential trace element exhibits important physiological functions and extensive

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Anisomycin alleviates Experimental Autoimmune Encephalolmylitis through the reduction of pro-inflammatory cytokines and Th17 cells, and the inhibition of GFAP and Iba1?

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Anisomycin alleviates Experimental Autoimmune Encephalolmyli...

第十届全国免疫学学术大会

作者： Manman Sun Song Liu Yuhua Ji Jia Xiao Jingfang Di Shan Zeng Jing Liu feiyue xing Institute of Tissue Transplantation and Immunology Department of Immunobiology Jinan University

Experimental autoimmune encephalomyelitis(EAE)is a T cell-mediated autoimmune disease of the central nervous *** previous studies showed that anisomycin could obviously inhibit the proliferation and differentiation of T cells and reduce the production of inflammatory *** the current study,an EAE model was established in C57BL/6female mice by myelin oligodendrocyte glycolprotein(MOG35-55).Anisomycin was used to treat the EAE-bearing mice to explore its therapeutic effect and *** mouse was subcutaneously immunized with 200μg of MOG35-55emulsified in CFA containing 5 mg/ml TB,and immediately injected intraperitoneally with pertussis ***,the mouse was administered with 400 ng of pertussis toxin once *** clinical signs in the anisomycin-treated mice were much slighter than those in the EAE-bearing *** maximum clinical sore in the EAE mice was 4.0 in the fastigium,but reduced to 2.0 by the treatment of *** maximum clinical score in the EAE mice was 3.0 in the paracmasis,but reduced to 1.5 by the treatment of anisomycin as *** with the EAE group,the demyelination of white matters and perivascular inflammatory infiltration appearing"sleeve-like"were reduced in the brain and spinal cord by the treatment of anisomycin,following the attenuation of the pro-inflammatory cytokines and chemokines as well as Th17 ***,the level of IL-17F did not significantly change dislike *** were regularities between the observed parameters and the clinical *** results indicate that anisomycin can extend the latent period in EAE-bearing mice,shorten the process of EAE progress,and reduce the pathological injury of the brain and spinal cord tissues,which involves the decreases of the pro-inflammatory cytokines and chemokines as well as Th17 cells,followed by the inhibition of GFAP and Iba1.

关键词： anisomycin GFAP Iba1 cytokine Th17 cell Experimental Autoimmune Encephalomyelitis

Jagged-1–Hes-1 signaling inhibits the differentiation of Th17 cells

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Jagged-1–Hes-1 signaling inhibits the differentiation of Th...

第八届全国免疫学学术大会

作者： Pengtao You Chengquan Mao Zhencheng Chen Xijian Lu Jingfang Di Shan Zeng Jing Liu feiyue xing Institute of Tissue Transplantation and Immunology Department of Immunobiology Jinan University

Background:Notch signaling plays an important role in differentiation of T ***, little is known as to action of it in differentiation of Th17 cell ***:In this study, a soluble Jagged-1/Fc chimera protein(Jagged-1) was directly used to activate Jagged-1–Notch signaling, while Hes-1-gargeting siRNA was used to knock down Hes-1 gene to investigate effect of Jagged-1–Hes-1 signaling on the differentiation of CD4+ T cells into Th17 *** and Results:The results showed that Jagged-1 could promote the expression of Hes-1 and Deltex-1 mRNAs and the expression of NICD, Hes-1 and Deltex-1 proteins, which might be significantly blocked by DAPT, a specific inhibitor of Notch ***-1 or Hes-1-si R NA resulted in the markedly decreased in situ expression of RORγt in the CD4+ T cells induced by IL-6 plus TGF-β.Flow cytometric analysis showed the reduction of IL-17 production in CD4+ T cells by Jagged-1, but the enhancement of it by Hes-1-gargeting *** level of IL-10 produced by the treated cells was also enhanced, whereas the expression of IL-17 was prominently attenuated, which could be offset by anti-Jagged-1 antibody or ***:The results indicate that Jagged-1–Hes-1 signaling can suppress the skewing of CD4+ T cells toward Th17 cells via RORγt, for which hes-1 may be crucial.

关键词： Jagged-1 Hes-1 siRNA Th17 differentiation