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60. Chemotherapeutic Tumor Microparticles Elicit a Neutrophil Response Targeting Malignant Pleural Effusions

Author

Xu, Pingwei, primary, Tang, Ke, additional, Ma, Jingwei, additional, Zhang, Huafeng, additional, Wang, Dianheng, additional, Zhu, Liyan, additional, Chen, Jie, additional, Wei, Keke, additional, Liu, Jincheng, additional, Fang, Haiqing, additional, Tang, Liang, additional, Zhang, Yi, additional, Xie, Jing, additional, Liu, Yuying, additional, Meng, Rui, additional, Liu, Li, additional, Dong, Xiaorong, additional, Yang, Kunyu, additional, Wu, Gang, additional, Ma, Fei, additional, and Huang, Bo, additional

Published
2020
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61. Ketogenesis-generated β-hydroxybutyrate is an epigenetic regulator of CD8+ T-cell memory development

Author

Zhang, Huafeng, primary, Tang, Ke, additional, Ma, Jingwei, additional, Zhou, Li, additional, Liu, Jincheng, additional, Zeng, Liping, additional, Zhu, Liyan, additional, Xu, Pingwei, additional, Chen, Jie, additional, Wei, Keke, additional, Liang, Xiaoyu, additional, Lv, Jiadi, additional, Xie, Jing, additional, Liu, Yuying, additional, Wan, Yonghong, additional, and Huang, Bo, additional

Published
2019
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64. Autologous tumor cell–derived microparticle-based targeted chemotherapy in lung cancer patients with malignant pleural effusion

Author

Guo, Mengfei, primary, Wu, Feng, additional, Hu, Guorong, additional, Chen, Lian, additional, Xu, Juanjuan, additional, Xu, Pingwei, additional, Wang, Xuan, additional, Li, Yumei, additional, Liu, Shuqing, additional, Zhang, Shuai, additional, Huang, Qi, additional, Fan, Jinshuo, additional, Lv, Zhilei, additional, Zhou, Mei, additional, Duan, Limin, additional, Liao, Tingting, additional, Yang, Guanghai, additional, Tang, Ke, additional, Liu, Bifeng, additional, Liao, Xiaofei, additional, Tao, Xiaonan, additional, and Jin, Yang, additional

Published
2019
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65. Mechanisms by Which Dendritic Cells Present Tumor Microparticle Antigens to CD8+ T Cells

Author

Ma, Jingwei, primary, Wei, Keke, additional, Zhang, Huafeng, additional, Tang, Ke, additional, Li, Fei, additional, Zhang, Tianzhen, additional, Liu, Junwei, additional, Xu, Pingwei, additional, Yu, Yuandong, additional, Sun, Weiwei, additional, Zhu, LiYan, additional, Chen, Jie, additional, Zhou, Li, additional, Liang, Xiaoyu, additional, Lv, Jiadi, additional, Fiskesund, Roland, additional, Liu, Yuying, additional, and Huang, Bo, additional

Published
2018
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66. Circulating Tumor Microparticles Promote Lung Metastasis by Reprogramming Inflammatory and Mechanical Niches via a Macrophage-Dependent Pathway

Author

Zhang, Huafeng, primary, Yu, Yuandong, additional, Zhou, Li, additional, Ma, Jingwei, additional, Tang, Ke, additional, Xu, Pingwei, additional, Ji, Tiantian, additional, Liang, Xiaoyu, additional, Lv, Jiadi, additional, Dong, Wenqian, additional, Zhang, Tianzhen, additional, Chen, Degao, additional, Xie, Jing, additional, Liu, Yuying, additional, and Huang, Bo, additional

Published
2018
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69. A Pck1-directed glycogen metabolic program regulates formation and maintenance of memory CD8+ T cells

Author

Ma, Ruihua, primary, Ji, Tiantian, additional, Zhang, Huafeng, additional, Dong, Wenqian, additional, Chen, Xinfeng, additional, Xu, Pingwei, additional, Chen, Degao, additional, Liang, Xiaoyu, additional, Yin, Xiaonan, additional, Liu, Yuying, additional, Ma, Jingwei, additional, Tang, Ke, additional, Zhang, Yi, additional, Peng, Yue’e, additional, Lu, Jinzhi, additional, Qin, Xiaofeng, additional, Cao, Xuetao, additional, Wan, Yonghong, additional, and Huang, Bo, additional

Published
2017
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70. Chemotherapeutic tumor microparticles combining low-dose irradiation reprogram tumor-promoting macrophages through a tumor-repopulating cell-curtailing pathway

Author

Sun, Yanling, primary, Zheng, Zu'an, additional, Zhang, Huafeng, additional, Yu, Yuandong, additional, Ma, Jingwei, additional, Tang, Ke, additional, Xu, Pingwei, additional, Ji, Tiantian, additional, Liang, Xiaoyu, additional, Chen, Degao, additional, Jin, Xun, additional, Zhang, Tianzhen, additional, Long, Zhixiong, additional, Liu, Yuying, additional, and Huang, Bo, additional

Published
2017
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72. Ketogenesis-generated β-hydroxybutyrate is an epigenetic regulator of CD8+T-cell memory development

Author

Zhang, Huafeng, Tang, Ke, Ma, Jingwei, Zhou, Li, Liu, Jincheng, Zeng, Liping, Zhu, Liyan, Xu, Pingwei, Chen, Jie, Wei, Keke, Liang, Xiaoyu, Lv, Jiadi, Xie, Jing, Liu, Yuying, Wan, Yonghong, and Huang, Bo

Abstract

Glycogen has long been considered to have a function in energy metabolism. However, our recent study indicated that glycogen metabolism, directed by cytosolic phosphoenolpyruvate carboxykinase Pck1, controls the formation and maintenance of CD8+memory T (Tmem) cells by regulating redox homeostasis1. This unusual metabolic program raises the question of how Pck1 is upregulated in CD8+Tmemcells. Here, we show that mitochondrial acetyl coenzyme A is diverted to the ketogenesis pathway, which indirectly regulates Pck1expression. Mechanistically, ketogenesis-derived β-hydroxybutyrate is present in CD8+Tmemcells; β-hydroxybutyrate epigenetically modifies Lys 9 of histone H3 (H3K9) of Foxo1and Ppargc1a(which encodes PGC-1α) with β-hydroxybutyrylation, upregulating the expression of these genes. As a result, FoxO1 and PGC-1α cooperatively upregulate Pck1expression, therefore directing the carbon flow along the gluconeogenic pathway to glycogen and the pentose phosphate pathway. These results reveal that ketogenesis acts as an unusual metabolic pathway in CD8+Tmemcells, linking epigenetic modification required for memory development.

Published
2020
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73. Sequential Regulation of Local Reactive Oxygen Species by Ir@Cu/Zn-MOF Nanoparticles for Promoting Infected Wound Healing

Author

Tian, Jinrong, Dong, Xing, Sabola, Eluby Esmie, Wang, Yuqi, Chen, Kai, Zhu, Meng, Dai, Bichun, Zhang, Shanshan, Guo, Feixia, Shi, Keqing, Chi, Junjie, and Xu, Pingwei

Abstract

Most antimicrobials treat wound infections by an oxidation effect, which is induced by the generation of reactive oxygen species (ROS). However, the potential harm of the prolonged high level of ROS should not be ignored. In this study, we presented a novel cascade-reaction nanoparticle, Ir@Cu/Zn-MOF, to effectively regulate the ROS level throughout the healing progress of the infected wound. The nanoparticles consisted of a copper/zinc-modified metal–organic framework (Cu/Zn-MOF) serving as the external structure and an inner core composed of Ir-PVP NPs, which were achieved through a process known as “bionic mineralization”. The released Cu2+and Zn2+from the shell structure contributed to the production of ROS, which acted as antimicrobial agents during the initial stage. With the disintegration of the shell, the Ir-PVP NP core was gradually released, exhibiting the property of multiple antioxidant enzyme activities, thereby playing an important role in clearing excessive ROS and alleviating oxidative stress. In a full-layer infected rat wound model, Ir@Cu/Zn-MOF nanoparticles presented exciting performance in promoting wound healing by clearing the bacteria and accelerating neovascularization as well as collagen deposition. This study provided a promising alternative for the repair of infected wounds.

Published
2024
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75. Reversing drug resistance of soft tumor-repopulating cells by tumor cell-derived chemotherapeutic microparticles

Author

Ma, Jingwei, primary, Zhang, Yi, additional, Tang, Ke, additional, Zhang, Huafeng, additional, Yin, Xiaonan, additional, Li, Yong, additional, Xu, Pingwei, additional, Sun, Yanling, additional, Ma, Ruihua, additional, Ji, Tiantian, additional, Chen, Junwei, additional, Zhang, Shuang, additional, Zhang, Tianzhen, additional, Luo, Shunqun, additional, Jin, Yang, additional, Luo, Xiuli, additional, Li, Chengyin, additional, Gong, Hongwei, additional, Long, Zhixiong, additional, Lu, Jinzhi, additional, Hu, Zhuowei, additional, Cao, Xuetao, additional, Wang, Ning, additional, Yang, Xiangliang, additional, and Huang, Bo, additional

Published
2016
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77. Upregulation of Cytosolic Phosphoenolpyruvate Carboxykinase Is a Critical Metabolic Event in Melanoma Cells That Repopulate Tumors

Author

Li, Yong, primary, Luo, Shunqun, additional, Ma, Ruihua, additional, Liu, Jing, additional, Xu, Pingwei, additional, Zhang, Huafeng, additional, Tang, Ke, additional, Ma, Jingwei, additional, Zhang, Yi, additional, Liang, Xiaoyu, additional, Sun, Yanling, additional, Ji, Tiantian, additional, Wang, Ning, additional, and Huang, Bo, additional

Published
2015
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78. A Pck1-directed glycogen metabolic program regulates formation and maintenance of memory CD8+T cells

Author

Ma, Ruihua, Ji, Tiantian, Zhang, Huafeng, Dong, Wenqian, Chen, Xinfeng, Xu, Pingwei, Chen, Degao, Liang, Xiaoyu, Yin, Xiaonan, Liu, Yuying, Ma, Jingwei, Tang, Ke, Zhang, Yi, Peng, Yue’e, Lu, Jinzhi, Zhang, Yi, Qin, Xiaofeng, Cao, Xuetao, Wan, Yonghong, and Huang, Bo

Abstract

CD8+memory T (Tm) cells are fundamental for protective immunity against infections and cancers1–5 . Metabolic activities are crucial in controlling memory T-cell homeostasis, but mechanisms linking metabolic signals to memory formation and survival remain elusive. Here we show that CD8+Tm cells markedly upregulate cytosolic phosphoenolpyruvate carboxykinase (Pck1), the hub molecule regulating glycolysis, tricarboxylic acid cycle and gluconeogenesis, to increase glycogenesis via gluconeogenesis. The resultant glycogen is then channelled to glycogenolysis to generate glucose-6-phosphate and the subsequent pentose phosphate pathway (PPP) that generates abundant NADPH, ensuring high levels of reduced glutathione in Tm cells. Abrogation of Pck1–glycogen–PPP decreases GSH/GSSG ratios and increases levels of reactive oxygen species (ROS), leading to impairment of CD8+Tm formation and maintenance. Importantly, this metabolic regulatory mechanism could be readily translated into more efficient T-cell immunotherapy in mouse tumour models. Glycogen metabolism controls memory T cells. Ma et al. show that the metabolic gene PCK1promotes glycogen formation, which is used in the pentose phosphate pathway, generating glutathione that is important for counteraction of ROS and thus promotion of memory T-cell maintenance, and resulting in improved antitumour immunity.

Published
2018
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81. Innate Immune Cell–Derived Microparticles Facilitate Hepatocarcinoma Metastasis by Transferring Integrin αMβ2 to Tumor Cells

Author

Ma, Jingwei, primary, Cai, Wenqian, additional, Zhang, Yi, additional, Huang, Chunmei, additional, Zhang, Huafeng, additional, Liu, Jing, additional, Tang, Ke, additional, Xu, Pingwei, additional, Katirai, Foad, additional, Zhang, Jianmin, additional, He, Wei, additional, Ye, Duyun, additional, Shen, Guan-Xin, additional, and Huang, Bo, additional

Published
2013
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83. Delivery of chemotherapeutic drugs in tumour cell-derived microparticles

Author

Tang, Ke, primary, Zhang, Yi, additional, Zhang, Huafeng, additional, Xu, Pingwei, additional, Liu, Jing, additional, Ma, Jingwei, additional, Lv, Meng, additional, Li, Dapeng, additional, Katirai, Foad, additional, Shen, Guan-Xin, additional, Zhang, Guimei, additional, Feng, Zuo-Hua, additional, Ye, Duyun, additional, and Huang, Bo, additional

Published
2012
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85. Validated HPLC method for the quantitative determination of CoQ10 in dog plasma and its application to a pharmacokinetic study.

Author

Yuan, Bo, Liu, Chunling, Xu, Pingwei, Lin, Lin, Pan, Cheng, Wang, Linglan, and Xu, Haiyan

Abstract

Coenzyme Q10 (CoQ10) is a naturally occurring compound located in all membranes throughout the cell. A rapid and sensitive HPLC method was developed to determine the concentration of CoQ10 in dog plasma using a surrogate matrix. Chromatographic separation was carried out on a Diamonsil C18 column with the UV detector set at 275 nm. Methanol-2-propanol (40:60, v/v) was used as a mobile phase delivered at a flow rate of 1.0 mL/min. Calibrators were prepared using blank plasma-K2HPO4 buffer (50 m m, pH 8.0)-saline (1:3:6, v/v/v) as surrogate matrix. It was shown that the surrogate matrix had similar properties to dog plasma for CoQ10 in extraction, freeze-thaw and stability. The assay was linear over the concentration range of 0.10-100 µg/mL. The intra- and inter-day precisions were within 13.3% in terms of relative standard deviation (RSD%) and the accuracy was within ±7.5% in terms of relative error. This simple and reproducible HPLC method with less plasma volume (0.4 mL) and adequate sensitivity was successfully applied to pharmacokinetic studies of CoQ10 in dogs and an investigation of the effect of CoQ10 formulation on CoQ10 baseline levels. Copyright © 2010 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Published
2011
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86. Mechanisms by Which Dendritic Cells Present Tumor Microparticle Antigens to CD8 + T Cells.

Author

Ma J, Wei K, Zhang H, Tang K, Li F, Zhang T, Liu J, Xu P, Yu Y, Sun W, Zhu L, Chen J, Zhou L, Liang X, Lv J, Fiskesund R, Liu Y, and Huang B

Subjects
Animals, B7-1 Antigen genetics, B7-2 Antigen genetics, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors genetics, Cancer Vaccines immunology, Cell Differentiation, Cells, Cultured, Endocytosis immunology, Female, Histocompatibility Antigens Class I immunology, Lysosomes physiology, Melanoma, Experimental, Mice, Mice, Inbred C57BL, Antigen Presentation, Antigens, Neoplasm immunology, CD8-Positive T-Lymphocytes immunology, Cell-Derived Microparticles immunology, Dendritic Cells immunology
Abstract

Tumor cell-derived microparticles (T-MP) contain tumor antigen profiles as well as innate signals, endowing them with vaccine potential; however, the precise mechanism by which DCs present T-MP antigens to T cells remains unclear. Here, we show that T-MPs activate a lysosomal pathway that is required for DCs presenting tumor antigens of T-MPs. DCs endocytose T-MPs to lysosomes, where T-MPs increase lysosomal pH from 5.0 to a peak of 8.5 via NOX2-catalyzed reactive oxygen species (ROS) production. This increased pH, coupled with T-MP-driven lysosomal centripetal migration, promotes the formation of MHC class I-tumor antigen peptide complexes. Concurrently, endocytosis of T-MPs results in the upregulation of CD80 and CD86. T-MP-increased ROS activate lysosomal Ca 2+ channel Mcoln2, leading to Ca 2+ release. Released Ca 2+ activates transcription factor EB (TFEB), a lysosomal master regulator that directly binds to CD80 and CD86 promoters, promoting gene expression. These findings elucidate a pathway through which DCs efficiently present tumor antigen from T-MPs to CD8 + T cells, potentiating T-MPs as a novel tumor cell-free vaccine with clinical applications. Cancer Immunol Res; 6(9); 1057-68. ©2018 AACR ., (©2018 American Association for Cancer Research.)

Published
2018
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87. Validated HPLC method for the quantitative determination of CoQ(10) in dog plasma and its application to a pharmacokinetic study.

Author

Yuan B, Liu C, Xu P, Lin L, Pan C, Wang L, and Xu H

Subjects
Animals, Dogs, Sensitivity and Specificity, Ubiquinone blood, Ubiquinone pharmacokinetics, Chromatography, High Pressure Liquid methods, Ubiquinone analogs & derivatives
Abstract

Coenzyme Q(10) (CoQ(10) ) is a naturally occurring compound located in all membranes throughout the cell. A rapid and sensitive HPLC method was developed to determine the concentration of CoQ(10) in dog plasma using a surrogate matrix. Chromatographic separation was carried out on a Diamonsil C(18) column with the UV detector set at 275 nm. Methanol-2-propanol (40:60, v/v) was used as a mobile phase delivered at a flow rate of 1.0 mL/min. Calibrators were prepared using blank plasma-K(2) HPO(4) buffer (50 mm, pH 8.0)-saline (1:3:6, v/v/v) as surrogate matrix. It was shown that the surrogate matrix had similar properties to dog plasma for CoQ(10) in extraction, freeze-thaw and stability. The assay was linear over the concentration range of 0.10-100 µg/mL. The intra- and inter-day precisions were within 13.3% in terms of relative standard deviation (RSD%) and the accuracy was within ±7.5% in terms of relative error. This simple and reproducible HPLC method with less plasma volume (0.4 mL) and adequate sensitivity was successfully applied to pharmacokinetic studies of CoQ(10) in dogs and an investigation of the effect of CoQ(10) formulation on CoQ(10) baseline levels., (Copyright © 2010 John Wiley & Sons, Ltd.)

Published
2011
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