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cAMP Modulates macrophage Development by Suppressing M-CSF-Induced maPKs Activation

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Cellular & Molecular Immunology 2008年第2期5卷 153-157页

作者： Ning Zhu Jian Cui Chunxia Qiao Yan Li yuanfang ma Jiyan Zhang Beifen Shen Department of Molecular Immunology Institute of Basic Medical Sciences Beijing 100850 China Laboratory of Cellular and Molecular Immunology Henan University Kaifeng China These authors contributed equally to this work

M-CSF is a key cytokine in macrophage development by inducing maPKs activation, and cAMP can inhibit maPKs activation induced by inflammatory stimuli. To explore the effects of cAMP on M-CSF-induced maPKs activation and on macrophage development, the model of bone marrow-derived murine macrophages （BMMs） was used. The effects of cAMP on M-CSF-induced maPKs activation were analyzed by Western blotting assay, and the effects of cAMP on CD14 and F4/80 expression during macrophage development were examined by FACS analysis. macrophage morphology showed the successful establishment of the model of macrophage development. Western blotting assay revealed that M-CSF activated ERK, JNK and p38 in both mature and immature macrophages, and cAMP inhibited M-CSF-induced ERK, JNK and p38 activation in a time-dependent manner. FACS analysis revealed that macrophage development was impaired with cAMP pretreatment. In conclusion, cAMP modulates macrophage development by suppressing M-CSF-induced maPKs activation. Cellular ＆ Molecular Immunology.

关键词： macrophage development M-CSF cAME maPKs

High-Affinity Decoy PD-1 Mutant Screened from an Epitope-Specific Cell Library

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Engineering 2021年第11期7卷 1557-1565页

作者： Hao Liu Chunxia Qiao Naijing Hu Zhihong Wang Jing Wang Jiannan Feng Beifen Shen yuanfang ma Longlong Luo State Key Laboratory of Toxicology and Medical Countermeasures Beijing Institute of Pharmacology and ToxicologyBeijing 100850China Joint National Laboratory for Antibody Drug Engineering The First Affiliated HospitalSchool of MedicineHenan UniversityKaifeng 475004China School of Life Science and Biopharmaceutics Shenyang Pharmaceutical UniversityShenyang 110016China School of Basic Medicine and Clinical Pharmacy China Pharmaceutical UniversityNanjing 210009China

Immunotherapy with anti-programmed cell death protein-1(PD-1)/programmed cell death ligand-1(PDL1)monoclonal antibodies has become routine in the treatment of many kinds of human cancers,such as lung cancer,intestinal cancer,and *** PD-1/PD-L1 pathway inhibits T cell activation in the micro-environment,making it an attractive target against ***-type(WT)PD-1 ectodomain has been shown to have difficulty blocking PD-1/PD-L1 mixture formation due to its low *** present work uses three-dimensional(3D)crystal complex structures to analyze the interaction by which PD-1 binds to PD-L1 or *** also reports on a theoretical study of the binding mode between PD-1 and its clinical antibody *** on the theoretical binding analysis of PD-1 and its ligands(i.e.,PD-L1 and PD-L2)or antibody(Opdivo),a small-content,epitope-oriented mammalian cell library was established for *** three rounds of cell sorting,the decoy PD-1 mutant 463,which presented a higher affinity than WT PD-1 to the PD-L1(the affinity has increased by almost three orders of magnitude)was screened *** exhibited an inhibitory effect against PD-1 to prevent it from forming mixtures with PD-L1,which was similar to the effect of the commercial anti-PD-L1 antibody atezolizumab(ATE).The median effective concentration(EC50)value of the decoy mutant was 0.031 μg·mL^(-1) in comparison with 0.063 μg·mL^(-1) for ATE;both values were much lower than that of WT PD-1,at 2.571 μg·mL^(-1).The 463 decoy mutant reversed the inhibitory function of PD-1 in T cell activation;furthermore,10 mg·kg^(-1) of 463 inhibited about 75%of tumor growth in vivo in a MC38 transgenic xenograft mice model,which was similar to the activity of *** interestingly,an even lower dose of 463(2 mg·kg^(-1))showed a better effect than 10 mg·kg^(-1) of WT *** work offers the decoy 463 with an improved curative effect,which holds potential to become a good option against PD-1/PD-L1-related cancers.

关键词： Decoy PD-1 PD-L1 mammalian cell library Epitope-oriented

Inhibitory activity of Bifidobacterium adolescent combined with cisplatin on melanoma in mice and its mechanism

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Frontiers of Medicine 2008年第2期2卷 186-190页

作者： Hongying HUANG Guangchao LIU Yijun QI Yaowu DU Jugao CHEN yuanfang ma Key Laboratory of Cellular and Molecular Immunology Institute for ImmunologyHenan UniversityKaifeng 475004China

The aim of this study is to explore inhibitory activity of Bifidobacterium adolescent combined with cis-platin on the growth of melanoma(B16)in mice and the underlying mechanism.C57 mice were inoculated with B16 cancer cells to construct mouse model of melanoma and treated with bifidobacterium adolescent combined with *** of inhibitory activity on the growth of melanoma(B16)were *** changes of the tumor were observed by HE staining.B16 cell cycles were examined on a flow *** prolif-eration was measured with MTT assay and the T-cell sub-set was measured by double marked *** bifidobacterium of 1010 cfu/L was injected,the ratio of inhibitory activity on the growth of melanoma(B16)reached 54%,which was similar to that of cisplatin *** ratio of inhibitory activity reached 74.45%when the mice were treated by bifidobacterium combined with *** staining shows that bifidobacterium inhibited B16 cell proliferation and enhanced the cisplatin`s killing activity on B16 *** results of flow cytometry demonstrated that B16 cell proliferation was arrested at G1 stage after treatment with *** B16 cell proliferation was arrested at S stage after treatment with *** CD4+percentage increased and the difference was significant compared with the normal group after treatment with bifidobacterium,indicating that T-cell immune activity was *** with bifidobacterium combined with cisplatin can enhance the inhibitory activity on the growth of melanoma(B16)of *** mechanism of the inhibitory activity on B16 cell proliferation is correlated with the enhanced immune activity in mice.

关键词： Bifidobacterium adolescent cisplatin mela-noma,experimental

Functional Identification of the Stable Transfection C5aR Cell Line Molt-4

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Cellular & Molecular Immunology 2007年第6期4卷 461-465页

作者： Chunmei Zhang Ruonan Xu Jianan Wang Gencheng Han Guojiang Chen Renxi Wang Huawei Wei Beifen Shen yuanfang ma Yan Li Institute of Basic Medical Sciences Beijing China Laboratory of Cellular and Molecular Immunology Henan University Kaifeng China

The complement C5 anaphylatoxin receptor is a member of the seven transmembrane-spanning G protein-coupled receptor superfamily that signals through Gcxi and Gtz16. C5aR is mostly expressed on neutrophils, macrophages and endothelial cells. C5a and C5aR interaction plays an important role in numerous biological effects such as in vivo cytokine storm which results in inflammatory damage. Considering the limitation of collection of human peripheral blood neutrophils and their short half life, the stably transfected cell line for studying the biological effects of C5aR is needed. In this study, we transfected C5aR gene into Molt-4 cell line and examined the function of ectopic C5aR. Our results showed stable expression of the C5aR in Molt-4 cell line and their interaction with human C5a induced ERKI/2 phosphorylation, Ca＋＋ influx. This stable transfected cell line may provide a useful tool for studying signal pathways related to C5a and C5aR interplay and antibody development specific for C5aR. Cellular ＆ Molecular Immunology.

关键词： complement C5a C5aR Molt-4

Characterization of a Novel Anti-DR5 Monoclonal Antibody WD1 with the Potential to Induce Tumor Cell Apoptosis

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Cellular & Molecular Immunology 2008年第1期5卷 55-60页

作者： Jing Wang Zhou Lin Chunxia Qiao Ming Lv Ming Yu He Xiao Qingyang Wang Liyan Wang Jiannan Feng Beifen Shen yuanfang ma Yan Li Laboratory of Cellular and Molecular Immunology Institute of Immunology Henan University Kaifeng China Institute of Basic Medical Sciences Beijing China These authors contributed equally to this work

TNF-related apoptosis-inducing ligand （TRAIL） is a TNF family member capable of inducing apoptosis. Death receptor 5 （DR 5） is a key receptor of TRAIL and plays an important role in TRAIL-induced apoptosis. To prepare monoclonal antibodies （mabs） against DR5, cDNA encoding soluble DR5 （sDR5） was firstly amplified by reverse transcriptase-polymerase chain reaction （RT-PCR） with specific primers, and then inserted into a prokaryotic expression vector pET-30a. The recombinant plasmid was expressed in Escherichia coli strain BL21 （DE3）, and sDR5 was purified by nickel affinity chromatography. As an antigen, sDR5 was used to immunize mice. Hybridomas secreting antibodies against sDR5 were identified. One positive done was selected to produce antibody, WD1. ELISA and immunofluorescence demonstrated that WD1 could bind recombinant sDR5 and membranebound DR5 （mDR5） on Jurkat and Molt-4 cells. ATPLite assays showed that Jurkat and Molt-4 cells were sensitive to the antibody in a dose dependent manner. The Annexin V/PI assays and Giemsa＇s staining both showed that WD1 could induce Jurkat cell apoptosis efficiently. Transient transfection of 293T cells and indirect immunofluorescence assay demonstrated that mab （WD1） couldn＇t cross-react with DR4. Our findings indicated that the novel antibody, WD1 could act as a direct agonist, bind DR5 characteristically, and initiate efficient apoptotic signaling and tumor regression. Thus, WD1 would be a leading candidate for potential cancer therapeutics. Cellular ＆ Molecular Immunology.

关键词： TRAIL death receptor 5 apoptosis monoclonal antibody ATPLite

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三维激光点云自动化建模思路探索

测绘通报 2022年第9期 119-122页

作者：马原放李海鹏贾光军北京市测绘设计研究院北京100038 城市空间信息工程北京市重点实验室北京100038

点云数据自动化应用时,尤其是三维自动化建模过程中,传统的点云自动化处理技术难以实现。点云自动化建模是一个复杂的过程,涉及对象识别、点云处理、参数化建模等多个领域。本文结合三维激光扫描技术,针对不同的项目和应用方向对三维模... 详细信息

点云数据自动化应用时,尤其是三维自动化建模过程中,传统的点云自动化处理技术难以实现。点云自动化建模是一个复杂的过程,涉及对象识别、点云处理、参数化建模等多个领域。本文结合三维激光扫描技术,针对不同的项目和应用方向对三维模型成果的不同需求,对现阶段各个行业和方向的三维模型成果及构建方法进行了汇总和分析,进一步提出了3种三维激光点云自动化建模的新思路和可行性分析,并分析了自动化建模思路的优势和应用方向。

关键词：三维激光扫描点云自动化建模逆向工程

维生素E琥珀酸酯增强DR5抗体对Raji和K562细胞的凋亡作用(英文)

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The Chinese-German Journal of Clinical Oncology 2012年第4期11卷 187-191页

作者： Jun Zhang Shulian Li Jingfang Du yuanfang ma Key Laboratory of Cellular and Molecular Immunology Institute of ImmunologyHenan UniversityKaifeng 475004China

Objective: The aim of our study was to detect whether Vitamin E Succinic Acid (VES) could regulate the expression level of DR5 in the cells and further elucidate the potential mechanisms involving that VES enhances the effect of mDRA-6 to eradicate leukemia Raji and K562 cells. Methods: MTT method was used to detect the growth inhibition of VES and mDRA-6 to Raji and K562 cells. Annexin V-FITC/PI double staining assay was used to analysis the apoptosis of leukemia cell. Flow cytometry was used to detect the cell surface DR5 expression. Immunoblotting technique was used to detect the DR5 protein expression. Results: MTT detection showed that 10 μmol/L mDRA-6 on the cell death rates of Raji and K562 cells were 21.98% and 5.23%, respectively. While increasing concentration of VES (5 μmol/L, 10 μmol/L, 20 μmol/L) and mDRA-6 both on the cell viability of Raji or K562 cells, the mortality of Raji cells elevated to 24.67%, 35.65% (P<0.01) and 40.22% (P<0.01), respectively. Similarly, the mortality of K562 cells increase to 6%, 7.89% (P<0.01) and 8.67% (P<0.01), respectively. To further specify the increased cell death rate induced by mDRA-6 and VES, the treated cells were analyzed by Annexin-V/PI staining assay. As shown in Fig. 1, the apoptosis rates of Raji and K562 cells treated with 2 μg/mL mDRA-6 for 12 h were 20.79% and 7.74%. Compared with this, the proportion of apoptotic cells increased upon exposure to 2 μg/mL mDRA-6 combination with 10 μmol/L VES, the apoptosis rates of Raji and K562 cells were 43.18% and 16.99%, respectively. To examine the anticancer effects of a combination strategy based on mDRA-6 and VES. We analyzed whether VES could elevated the expression level of DR5 on Raji and K562 cytomembrane by FACS. Interestingly, after treated with 10 μmol/L VES for 12 h, the expression level of DR5 on Raji and K562 cell surface increased from 50.66% to 70.08%, and 15.02% to 16.38%, respectively. Immune imprinting technology test showed that, different concentrat

关键词：白血病细胞诱导凋亡维生素E K562细胞丁二酸 Raji细胞免疫印迹技术 Annexin

The function of HSF1 in SV40T-antigen induced tumorigenesis

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The function of HSF1 in SV40T-antigen induced tumorigenesis

mDRA-6与尼美舒利对人肝癌细胞系SMMC-7721细胞的协同杀伤效应(英文)

中国解剖学会2013年年会

作者： Jiang Qiying Zhang zhi Hu Yanzhong ma yuanfang Medical College of Henan University

＜正＞Heat shock factor 1（HSF1）,a main regulator of the heat shock response in eukaryotes,can increase the survival in many pathophysiological *** observe the function of defective HSF1 expression in SV40T-antigen（SV40T-ag） induced *** colony formation assay,MTT assay,Flow cytometry,nude mouse subcutaneous engraft

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The Chinese-German Journal of Clinical Oncology 2008年第12期7卷 694-697页

作者： Jun Zhang Yingjie Liu Zengyi ma Jing wang Shulian Li Huiling Bai yuanfang ma Key Laboratory for Naturaldrug and Immunoengineering of Henan province Henan University Kaifeng475003China Institue of Immunology Medical college of Henan University Kaifeng 475003 China

Objective: The aim of this work was to evaluate anti-tumor effects of mDRA-6 plus nimesulide on a human hepatocellular cancer cell line, SMMC-7721, and study the main mechanisms. Methods: The DR5 receptor of SMMC-7721 cells was detected by flow cytometry (FCM). For further experimental application, SMMC-7721 cells were treated with proper dose of mDRA-6, nimesulide, or mDRA-6 plus 200 μmol/L nimesulide; untreated SMMC-7721 cells were comparably set as control. Cytotoxicity was tested by MTT assay; cell morphology was examined using Hoechst 33258 staining; and apoptosis was determined by FCM. Results: The positive rate of DR5 on SMMC-7721 was 95.0%. Either mDRA-6 or nimesulide alone induces SMMC-7721 cell death in a dose-dependent manner. Treatment of 1,600 ng/mL mDRA-6 for 12h led to a cell-death rate of 35.0%, while an increased cell-death rate (91.1%) was found under the same condition of mDRA-6 treatment supple- mented with 200 μmol/L nimesulide. Hoechst 33258 and Annexin V/PI staining confirmed apoptosis as the main cause of this anti-tumor response. Conclusion: Both mDRA-6 and nimesulide can induce apoptosis of SMMC-7721 cells, and they have synergistic anti-tumor activities against SMMC-7721.

关键词：肝癌癌细胞治疗疗效临床