14 results on '"Qin, Dengke"'
Search Results
2. CD24+ decidual stromal cells: a novel heterogeneous population with impaired regulatory T cells induction and potential association with recurrent miscarriage.
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Qin, Dengke, primary, Chen, Zechuan, additional, Deng, Xujing, additional, Liu, Xiaoshan, additional, Peng, Liying, additional, Li, Guohua, additional, Liu, Yuan, additional, Zhu, Xiuxian, additional, Ding, Qiuhong, additional, Zhang, Xiaoming, additional, and Bao, Shihua, additional
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- 2023
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3. Single-cell profiling reveals mechanisms of uncontrolled inflammation and glycolysis in decidual stromal cell subtypes in recurrent miscarriage
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Bao, Shihua, primary, Chen, Zechuan, additional, Qin, Dengke, additional, Xu, Huihui, additional, Deng, Xujing, additional, Zhang, Ruixiu, additional, Ma, Jiaqiang, additional, Lu, Zhouping, additional, Jiang, Shan, additional, and Zhang, Xiaoming, additional
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- 2022
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4. The peripheral and decidual immune cell profiles in women with recurrent pregnancy loss
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Qin, Dengke, primary, Xu, Huihui, additional, Chen, Zechuan, additional, Deng, Xujing, additional, Jiang, Shan, additional, Zhang, Xiaoming, additional, and Bao, Shihua, additional
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- 2022
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5. Emodin Suppresses the Migration and Invasion of Melanoma Cells
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Zhu Jingjing, Chuanlong Jia, Mingjie Yuan, Zhou Yiqun, Heng Wang, Qin Dengke, Wang Wanchen, Liang Chen, Tianyi Liu, Haiguang Zhao, Guo Yu, and Chi Liu
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0301 basic medicine ,Emodin ,Genes, myc ,Pharmaceutical Science ,Apoptosis ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Annexin ,Cell Line, Tumor ,medicine ,Humans ,Neoplasm Invasiveness ,Propidium iodide ,Rheum ,Melanoma ,Protein Kinase Inhibitors ,Wnt Signaling Pathway ,beta Catenin ,Cell Proliferation ,bcl-2-Associated X Protein ,Pharmacology ,Plant Extracts ,Cell growth ,Wnt signaling pathway ,General Medicine ,medicine.disease ,Antineoplastic Agents, Phytogenic ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,Matrix Metalloproteinase 9 ,Proto-Oncogene Proteins c-bcl-2 ,chemistry ,030220 oncology & carcinogenesis ,Cancer cell ,Cancer research ,Matrix Metalloproteinase 2 ,TCF Transcription Factors ,Phytotherapy - Abstract
Emodin (1,3,8-trihydroxy-6-methylanthraquinone), as an active ingredient in rhubarb roots and rhizomes, has been reported to possess various pharmacological properties including anti-tumor effects. Recent studies have confirmed that emodin inhibited cell proliferation and induced apoptosis of cancer cells. However, the inhibitory effect of emodin on the migration and invasion of melanoma cells and its underlying mechanism are still unclear. In the study, we observed the impercipient effects of emodin in B16F10 and A375 melanoma cells with strong metastatic abilities, focusing on the functions and mechanisms of migration and invasion of B16F10 and A375 melanoma cells. Cell counting kit-8 (CCK-8), colony formation test and Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining tests confirmed that emodin possessed anti-proliferative and pro-apoptotic activities in B16F10 and A375 cells. The inhibitory effects on the migration and invasion of B16F10 and A375 cells were proved by wound healing assay and Transwell methods. Moreover, immunofluorescence assay approved the decrease in protein expression of matrix metalloproteinas (MMP)-2/-9 by emodin, and Western blot analyses revealed that emodin could increase the Bax/Bcl-2 ratio and inhibit the MMP-2/-9 protein expression and Wnt/β-catenin pathway in a dose-depended manner. BML-284, as an agonist of Wnt/β-catenin signaling pathway, reversed the effects of emodin on cell growth, migration and invasion in B16F10 cells. These findings may suggest that emodin treatment can be a promising therapeutic strategy for melanoma with highly metastatic abilities.
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- 2021
6. Single-cell profiling reveals mechanisms of uncontrolled inflammation and glycolysis in decidual stromal cell subtypes in recurrent miscarriage.
- Author
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Bao, Shihua, Chen, Zechuan, Qin, Dengke, Xu, Huihui, Deng, Xujing, Zhang, Ruixiu, Ma, Jiaqiang, Lu, Zhouping, Jiang, Shan, and Zhang, Xiaoming
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RECURRENT miscarriage ,STROMAL cells ,GLYCOLYSIS ,RESEARCH & development ,KILLER cells - Abstract
Study Question: Do distinct subpopulations of decidual stromal cells (DSCs) exist and if so, are given subpopulations enriched in recurrent miscarriage (RM)?Summary Answer: Three subpopulations of DSCs were identified from which inflammatory DSCs (iDSCs) and glycolytic DSCs (glyDSCs) are significantly enriched in RM, with implicated roles in driving decidual inflammation and immune dysregulation.What Is Known Already: DSCs play crucial roles in establishing and maintaining a successful pregnancy; dysfunction of DSCs has been considered as one of the key reasons for the development of RM.Study Design, Size, Duration: We collected 15 early decidual samples from five healthy donors (HDs) and ten RM patients to perform single-cell RNA sequencing (scRNA-seq). A total of 43 RM patients and 37 HDs were enrolled in the validation cohort.Participants/materials, Setting, Methods: Non-immune cells and immune cells of decidual tissues were sorted by flow cytometry to perform scRNA-seq. We used tissue microarrays (TMA) to validate three distinct subpopulations of DSCs. The expression of inflammatory and glycolytic proteins by DSCs was validated by immunohistochemistry (IHC) and multiplex immunohistochemistry (mIHC). Different subsets of decidual NK (dNK) cells and macrophages were also validated by multicolor flow cytometry and mIHC. Cell ligand-receptor and spatial analyses between DSCs and immune cells were analyzed by mIHC.Main Results and the Role Of Chance: We classify the DSCs into three subtypes based on scRNA-seq data: myofibroblastic (myDSCs), inflammatory (iDSCs) and glycolytic (glyDSCs), with the latter two being significantly enriched in RM patients. The distribution patterns of DSC subtypes in the RM and HD groups were validated by mIHC. Single-cell analyses indicate that the differentiation of iDSCs and glyDSCs may be coupled with the degrees of hypoxia. Consequently, we propose a pathological model in which a vicious circle is formed and fueled by hypoxic stress, uncontrolled inflammation and aberrant glycolysis. Furthermore, our results show that the inflammatory SPP1+ macrophages and CD18+ dNK cells are preferentially increased in the decidua of RM patients. Cell ligand-receptor and mIHC spatial analyses uncovered close interactions between pathogenic DSCs and inflammatory SPP1+ macrophages and CD18+ NK cells in RM patients.Large Scale Data: The raw single-cell sequence data reported in this paper were deposited at the National Omics Data Encyclopedia (www.biosino.org), under the accession number OEP002901.Limitations, Reasons For Caution: The number of decidual samples for scRNA-seq was limited and in-depth functional studies on DSCs are warranted in future studies.Wider Implications Of the Findings: Identification of three DSC subpopulations opens new avenues for further investigation of their roles in RM patients.Study Funding/competing Interest(s): This study was supported by the Strategic Priority Research Program (No. XDB29030302), Frontier Science Key Research Project (QYZDB-SSW-SMC036), Chinese Academy of Sciences; National Key Research and Development Program of China (2021YFE0200600), National Natural Science Foundation of China (No. 31770960), Shanghai Municipal Science and Technology Major Project (No. 2019SHZDZX02, HS2021SHZX001), and Shanghai Committee of Science and Technology (17411967800). All authors report no conflict of interest. [ABSTRACT FROM AUTHOR]- Published
- 2023
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7. Emodin inhibits the proliferation and migration of B16F10 cells and induces their apoptosis
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Qin Dengke, Bi Bo, Ping Yang, Guo Yu, Liang Chen, Heng Wang, Zhou Yiqun, Haiguang Zhao, Mingjie Yuan, Chuanlong Jia, Tianyi Liu, Chi Liu, Wang Wanchen, and Zhu Jingjing
- Subjects
Cancer Research ,Emodin ,B16F10 ,proliferation ,apoptosis ,migration ,Cell biology ,chemistry.chemical_compound ,Oncology ,chemistry ,Apoptosis ,Radiology, Nuclear Medicine and imaging ,Original Article - Abstract
Background Emodin, extracted from the rhizomes of various Chinese herbs, is a natural anthraquinone derivative with the formula C15H10O5. Many recent studies have shown that emodin has an antitumour effect. In this study, emodin was investigated in vitro to observe its effect on the proliferation, migration, and apoptosis of the B16F10 melanoma cell line. Methods B16F10 cells were treated with 20, 40, 60, or 80 µM emodin for 24 h. A Cell Counting Kit-8 (CCK-8) was used to measure the effect of emodin on cell proliferation. After 24 h of emodin treatment, a scratch test was used to detect the wound healing rate of each group. A Transwell test was used to measure the effect of emodin on cell migration ability. The apoptosis rate of the B16F10 cells was determined by a TUNEL assay. The expression of caspase-3 was measured by western blot analysis. Results Compared with the control group, emodin significantly inhibited the proliferation and migration of the B16F10 cells in a concentration-dependent manner. Emodin also inhibited the migration of the B16F10 cells and induced their apoptosis. Conclusions Emodin can effectively suppress the viability and migration of B16F10 cells and may induce apoptosis through the mitochondrial pathway or death receptor-mediated pathway.
- Published
- 2020
8. Conversion of Amorphous MOF Microspheres into a Nickel Phosphate Battery-Type Electrode Using the “Anticollapse” Two-Step Strategy
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Zhang, Haobing, primary, Mei, Hao, additional, Qin, Dengke, additional, Li, Ziyi, additional, Hou, Zheyuan, additional, Lu, Xiaoqing, additional, Xu, Ben, additional, and Sun, Daofeng, additional
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- 2021
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9. Emodin Suppresses the Migration and Invasion of Melanoma Cells
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Liu, Chi, primary, Chen, Liang, additional, Wang, Wanchen, additional, Qin, Dengke, additional, Jia, Chuanlong, additional, Yuan, Mingjie, additional, Wang, Heng, additional, Guo, Yu, additional, Zhu, Jingjing, additional, Zhou, Yiqun, additional, Zhao, Haiguang, additional, and Liu, Tianyi, additional
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- 2021
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10. Emodin inhibits the proliferation and migration of B16F10 cells and induces their apoptosis
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Yuan, Mingjie, primary, Chen, Liang, additional, Wang, Wanchen, additional, Qin, Dengke, additional, Jia, Chuanlong, additional, Liu, Chi, additional, Wang, Heng, additional, Zhu, Jingjing, additional, Guo, Yu, additional, Zhou, Yiqun, additional, Yang, Ping, additional, Zhao, Haiguang, additional, Liu, Tianyi, additional, and Bi, Bo, additional
- Published
- 2020
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11. BMP2/7 heterodimer enhances osteogenic differentiation of rat BMSCs via ERK signaling compared with respective homodimers
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Miao, Chunlei, primary, Qin, Dengke, additional, Cao, Peigang, additional, Lu, Ping, additional, Xia, Yutong, additional, Li, Mengjiao, additional, Sun, Miao, additional, Zhang, Wei, additional, Yang, Fanghong, additional, Zhang, Yingjie, additional, Tang, Shengjian, additional, Liu, Tianyi, additional, and Liu, Fangjun, additional
- Published
- 2018
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12. Rapamycin Protects Skin Fibroblasts from Ultraviolet B-Induced Photoaging by Suppressing the Production of Reactive Oxygen Species
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Runjian Ren, Liang Chen, Qin Dengke, Bi Bo, Zhu Jingjing, Xinyuan Wu, Ningwen Zhu, Ping Yang, Yongzhou Lu, Guo Yu, Tianyi Liu, Chuanlong Jia, Yang Qingjian, and Zhou Yiqun
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0301 basic medicine ,Male ,Cell cycle checkpoint ,Physiology ,DNA damage ,Cell Survival ,Ultraviolet Rays ,Photoaging ,Cell morphology ,lcsh:Physiology ,lcsh:Biochemistry ,03 medical and health sciences ,Mice ,medicine ,Autophagy ,Animals ,lcsh:QD415-436 ,Rapamycin ,Cells, Cultured ,Cellular Senescence ,Cell Proliferation ,chemistry.chemical_classification ,Sirolimus ,Reactive oxygen species ,lcsh:QP1-981 ,Cell growth ,Chemistry ,ROS ,Cell Cycle Checkpoints ,Fibroblasts ,medicine.disease ,Cell biology ,Skin Aging ,Mice, Inbred C57BL ,030104 developmental biology ,Female ,Uvb ,Reactive Oxygen Species ,Sunscreening Agents ,Intracellular - Abstract
Background/Aims: Ultraviolet B (UVB) irradiation alters multiple molecular pathways in the skin, thereby inducing skin photoaging. Murine dermal fibroblasts (MDFs) were subjected to a series of 4 sub-cytotoxic UVB doses (120 mJ/cm2), resulting in changes in cell shape, DNA damage, cell cycle arrest, extracellular matrix variations, reactive oxygen species (ROS) generation, and alterations in major intracellular antioxidant and cellular autophagy levels. Rapamycin (RAPA) is a new macrolide immunosuppressive agent that is primarily used in oncology, cardiology, and transplantation medicine and has been found to extend the lifespan of genetically heterogeneous mice. Several studies have shown that RAPA may have anti-aging effects in cells and organisms. Thus, in this study, we explored the effects and mechanisms of RAPA against the photoaging process using a well-established cellular photoaging model. Methods: We developed a stress-induced premature senescence (SIPS) model through repeated exposure of MDFs to ultraviolet B (UVB) irradiation. The cells were cultured in the absence or presence of RAPA for 48 h. Senescent phenotypes were assessed by examining cell viability, cell morphology, senescence-associated β-galactosidase (SA-β-gal) expression, cell cycle progression, intracellular ROS production, matrix metalloproteinase (MMP) synthesis and degradation, extracellular matrix (ECM) component protein expression, alterations in major intracellular antioxidant levels, and the cellular autophagy level. Results: Compared with the UVB group, pretreatment with RAPA (5 µM) significantly decreased the staining intensity and percentage of SA-β-gal-positive cells and preserved the elongated cell shape. Moreover, cells pretreated with RAPA showed inhibition of the reduction in the type I collagen content by blocking the UVB-induced upregulation of MMP expression. RAPA also decreased photoaging cell cycle arrest and downregulated p53 and p21 expression. RAPA application significantly attenuated irradiation-induced ROS release by modulating intracellular antioxidants and increasing the autophagy level. Conclusions: Our study demonstrated that RAPA elicited oxidative damage in vitro by reducing ROS accumulation in photoaged fibroblasts. The anti-aging effect can be attributed to the maintenance of normal antioxidant and cellular autophagy levels. However, determination of the definitive mechanism requires further study.
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- 2017
13. BMP2/7 heterodimer enhances osteogenic differentiation of rat BMSCs via ERK signaling compared with respective homodimers.
- Author
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Miao, Chunlei, Qin, Dengke, Cao, Peigang, Lu, Ping, Xia, Yutong, Li, Mengjiao, Sun, Miao, Zhang, Wei, Yang, Fanghong, Zhang, Yingjie, Tang, Shengjian, Liu, Tianyi, and Liu, Fangjun
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- 2019
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14. Rapamycin Protects Skin Fibroblasts from Ultraviolet B-Induced Photoaging by Suppressing the Production of Reactive Oxygen Species.
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Qin D, Ren R, Jia C, Lu Y, Yang Q, Chen L, Wu X, Zhu J, Guo Y, Yang P, Zhou Y, Zhu N, Bi B, and Liu T
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- Animals, Cell Cycle Checkpoints drug effects, Cell Cycle Checkpoints radiation effects, Cell Proliferation drug effects, Cell Proliferation radiation effects, Cell Survival drug effects, Cell Survival radiation effects, Cells, Cultured, Female, Fibroblasts cytology, Fibroblasts metabolism, Male, Mice, Mice, Inbred C57BL, Reactive Oxygen Species metabolism, Skin Aging drug effects, Skin Aging radiation effects, Cellular Senescence drug effects, Cellular Senescence radiation effects, Fibroblasts drug effects, Fibroblasts radiation effects, Sirolimus pharmacology, Sunscreening Agents pharmacology, Ultraviolet Rays adverse effects
- Abstract
Background/aims: Ultraviolet B (UVB) irradiation alters multiple molecular pathways in the skin, thereby inducing skin photoaging. Murine dermal fibroblasts (MDFs) were subjected to a series of 4 sub-cytotoxic UVB doses (120 mJ/cm2), resulting in changes in cell shape, DNA damage, cell cycle arrest, extracellular matrix variations, reactive oxygen species (ROS) generation, and alterations in major intracellular antioxidant and cellular autophagy levels. Rapamycin (RAPA) is a new macrolide immunosuppressive agent that is primarily used in oncology, cardiology, and transplantation medicine and has been found to extend the lifespan of genetically heterogeneous mice. Several studies have shown that RAPA may have anti-aging effects in cells and organisms. Thus, in this study, we explored the effects and mechanisms of RAPA against the photoaging process using a well-established cellular photoaging model., Methods: We developed a stress-induced premature senescence (SIPS) model through repeated exposure of MDFs to ultraviolet B (UVB) irradiation. The cells were cultured in the absence or presence of RAPA for 48 h. Senescent phenotypes were assessed by examining cell viability, cell morphology, senescence-associated β-galactosidase (SA-β-gal) expression, cell cycle progression, intracellular ROS production, matrix metalloproteinase (MMP) synthesis and degradation, extracellular matrix (ECM) component protein expression, alterations in major intracellular antioxidant levels, and the cellular autophagy level., Results: Compared with the UVB group, pretreatment with RAPA (5 µM) significantly decreased the staining intensity and percentage of SA-β-gal-positive cells and preserved the elongated cell shape. Moreover, cells pretreated with RAPA showed inhibition of the reduction in the type I collagen content by blocking the UVB-induced upregulation of MMP expression. RAPA also decreased photoaging cell cycle arrest and downregulated p53 and p21 expression. RAPA application significantly attenuated irradiation-induced ROS release by modulating intracellular antioxidants and increasing the autophagy level., Conclusions: Our study demonstrated that RAPA elicited oxidative damage in vitro by reducing ROS accumulation in photoaged fibroblasts. The anti-aging effect can be attributed to the maintenance of normal antioxidant and cellular autophagy levels. However, determination of the definitive mechanism requires further study., (© 2018 The Author(s). Published by S. Karger AG, Basel.)
- Published
- 2018
- Full Text
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