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4. Role of STAT3‐FOXO3 Signaling in the Modulation of Neuroplasticity by PD‐L1‐HGF‐Decorated Mesenchymal Stem Cell‐Derived Exosomes in a Murine Stroke Model.

Author

Lin, Syuan‐Ling, Chang, Yi‐Wen, Lee, Wei, Chiang, Chih‐Sheng, Liu, Shih‐Ping, Lee, Hsu‐Tung, Jeng, Long‐Bin, and Shyu, Woei‐Cherng

Abstract

The limited therapeutic strategies available for stroke leave many patients disabled for life. This study assessed the potential of programmed death‐ligand 1 (PD‐L1) and hepatocyte growth factor (HGF)‐engineered mesenchymal stem cell‐derived exosomes (EXO‐PD‐L1‐HGF) in enhancing neurological recovery post‐stroke. EXO‐PD‐L1‐HGF, which efficiently endocytosed into target cells, significantly diminishes the H2O2‐induced neurotoxicity and increased the antiapoptotic proteins in vitro. EXO‐PD‐L1‐HGF attenuates inflammation by inhibiting T‐cell proliferation and increasing the number of CD8+CD122+IL‐10+ regulatory T cells. Intravenous injection of EXO‐PD‐L1‐HGF could target stromal cell‐derived factor‐1α (SDF‐1α+) cells over the peri‐infarcted area of the ischemic brain through CXCR4 upregulation and accumulation in neuroglial cells post‐stroke. EXO‐PD‐L1‐HGF facilitates endogenous nestin+ neural progenitor cell (NPC)‐induced neurogenesis via STAT3‐FOXO3 signaling cascade, which plays a pivotal role in cell survival and neuroprotection, thereby mitigating infarct size and enhancing neurological recovery in a murine stroke model. Moreover, increasing populations of the immune‐regulatory CD19+IL‐10+ and CD8+CD122+IL‐10+ cells, together with reducing populations of proinflammatory cells, created an anti‐inflammatory microenvironment in the ischemic brain. Thus, innovative approaches employing EXO‐PD‐L1‐HGF intervention, which targets SDF‐1α+ expression, modulates the immune system, and enhances the activation of resident nestin+ NPCs, might significantly alter the brain microenvironment and create a niche conducive to inducing neuroplastic regeneration post‐stroke. [ABSTRACT FROM AUTHOR]

Published
2024
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10. Supplementary Figure 2 from miR326 Maturation Is Crucial for VEGF-C–Driven Cortactin Expression and Esophageal Cancer Progression

Author

Hong, Chih-Chen, primary, Chen, Pai-Sheng, primary, Chiou, Jean, primary, Chiu, Ching-Feng, primary, Yang, Ching-Yao, primary, Hsiao, Michael, primary, Chang, Yi-Wen, primary, Yu, Yang-Hao, primary, Hung, Mien-Chie, primary, Hsu, Nai-Wen, primary, Shiah, Shine-Gwo, primary, Hsu, Nan-Yung, primary, and Su, Jen-Liang, primary

Published
2023
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12. Supplementary Figures 1-4 from FOXO3a-Dependent Mechanism of E1A-Induced Chemosensitization

Author

Su, Jen-Liang, primary, Cheng, Xiaoyun, primary, Yamaguchi, Hirohito, primary, Chang, Yi-Wen, primary, Hou, Chao-Feng, primary, Lee, Dung-Fang, primary, Ko, How-Wen, primary, Hua, Kuo-Tai, primary, Wang, Ying-Nai, primary, Hsiao, Michael, primary, Chen, PoShen B., primary, Hsu, Jung-Mao, primary, Bast, Robert C., primary, Hortobagyi, Gabriel N., primary, and Hung, Mien-Chie, primary

Published
2023
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17. Supplementary Information from miR326 Maturation Is Crucial for VEGF-C–Driven Cortactin Expression and Esophageal Cancer Progression

Author

Hong, Chih-Chen, primary, Chen, Pai-Sheng, primary, Chiou, Jean, primary, Chiu, Ching-Feng, primary, Yang, Ching-Yao, primary, Hsiao, Michael, primary, Chang, Yi-Wen, primary, Yu, Yang-Hao, primary, Hung, Mien-Chie, primary, Hsu, Nai-Wen, primary, Shiah, Shine-Gwo, primary, Hsu, Nan-Yung, primary, and Su, Jen-Liang, primary

Published
2023
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20. Data from FOXO3a-Dependent Mechanism of E1A-Induced Chemosensitization

Author

Su, Jen-Liang, primary, Cheng, Xiaoyun, primary, Yamaguchi, Hirohito, primary, Chang, Yi-Wen, primary, Hou, Chao-Feng, primary, Lee, Dung-Fang, primary, Ko, How-Wen, primary, Hua, Kuo-Tai, primary, Wang, Ying-Nai, primary, Hsiao, Michael, primary, Chen, PoShen B., primary, Hsu, Jung-Mao, primary, Bast, Robert C., primary, Hortobagyi, Gabriel N., primary, and Hung, Mien-Chie, primary

Published
2023
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22. Supplementary Figure 1 from miR326 Maturation Is Crucial for VEGF-C–Driven Cortactin Expression and Esophageal Cancer Progression

Author

Hong, Chih-Chen, primary, Chen, Pai-Sheng, primary, Chiou, Jean, primary, Chiu, Ching-Feng, primary, Yang, Ching-Yao, primary, Hsiao, Michael, primary, Chang, Yi-Wen, primary, Yu, Yang-Hao, primary, Hung, Mien-Chie, primary, Hsu, Nai-Wen, primary, Shiah, Shine-Gwo, primary, Hsu, Nan-Yung, primary, and Su, Jen-Liang, primary

Published
2023
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24. Supplementary Figure 5 from miR326 Maturation Is Crucial for VEGF-C–Driven Cortactin Expression and Esophageal Cancer Progression

Author

Hong, Chih-Chen, primary, Chen, Pai-Sheng, primary, Chiou, Jean, primary, Chiu, Ching-Feng, primary, Yang, Ching-Yao, primary, Hsiao, Michael, primary, Chang, Yi-Wen, primary, Yu, Yang-Hao, primary, Hung, Mien-Chie, primary, Hsu, Nai-Wen, primary, Shiah, Shine-Gwo, primary, Hsu, Nan-Yung, primary, and Su, Jen-Liang, primary

Published
2023
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25. Supplementary Figure Legends 1-4 from FOXO3a-Dependent Mechanism of E1A-Induced Chemosensitization

Author

Su, Jen-Liang, primary, Cheng, Xiaoyun, primary, Yamaguchi, Hirohito, primary, Chang, Yi-Wen, primary, Hou, Chao-Feng, primary, Lee, Dung-Fang, primary, Ko, How-Wen, primary, Hua, Kuo-Tai, primary, Wang, Ying-Nai, primary, Hsiao, Michael, primary, Chen, PoShen B., primary, Hsu, Jung-Mao, primary, Bast, Robert C., primary, Hortobagyi, Gabriel N., primary, and Hung, Mien-Chie, primary

Published
2023
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26. Supplementary Figure 3 from miR326 Maturation Is Crucial for VEGF-C–Driven Cortactin Expression and Esophageal Cancer Progression

Author

Hong, Chih-Chen, primary, Chen, Pai-Sheng, primary, Chiou, Jean, primary, Chiu, Ching-Feng, primary, Yang, Ching-Yao, primary, Hsiao, Michael, primary, Chang, Yi-Wen, primary, Yu, Yang-Hao, primary, Hung, Mien-Chie, primary, Hsu, Nai-Wen, primary, Shiah, Shine-Gwo, primary, Hsu, Nan-Yung, primary, and Su, Jen-Liang, primary

Published
2023
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28. Supplementary Figure 4 from miR326 Maturation Is Crucial for VEGF-C–Driven Cortactin Expression and Esophageal Cancer Progression

Author

Hong, Chih-Chen, primary, Chen, Pai-Sheng, primary, Chiou, Jean, primary, Chiu, Ching-Feng, primary, Yang, Ching-Yao, primary, Hsiao, Michael, primary, Chang, Yi-Wen, primary, Yu, Yang-Hao, primary, Hung, Mien-Chie, primary, Hsu, Nai-Wen, primary, Shiah, Shine-Gwo, primary, Hsu, Nan-Yung, primary, and Su, Jen-Liang, primary

Published
2023
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35. Büchi Store: An Open Repository of Büchi Automata

Author

Tsay, Yih-Kuen, Tsai, Ming-Hsien, Chang, Jinn-Shu, Chang, Yi-Wen, Hutchison, David, Series editor, Kanade, Takeo, Series editor, Kittler, Josef, Series editor, Kleinberg, Jon M., Series editor, Mattern, Friedemann, Series editor, Mitchell, John C., Series editor, Naor, Moni, Series editor, Nierstrasz, Oscar, Series editor, Pandu Rangan, C., Series editor, Steffen, Bernhard, Series editor, Sudan, Madhu, Series editor, Terzopoulos, Demetri, Series editor, Tygar, Doug, Series editor, Vardi, Moshe Y., Series editor, Weikum, Gerhard, Series editor, Abdulla, Parosh Aziz, editor, and Leino, K. Rustan M., editor

Published
2011
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36. Effect of Loading Devices on Muscle Activation in Squat and Lunge.

Author

Wu, Hong-Wen, Tsai, Cheng-Feng, Liang, Kai-Han, and Chang, Yi-Wen

Subjects
SKELETAL muscle physiology, ANALYSIS of variance, EXERCISE, EXERCISE physiology, LONGITUDINAL method, MUSCLE strength, T-test (Statistics), BODY movement, CROSS-sectional method, DATA analysis software, RESISTANCE training
Abstract

Context: Squats and lunges are common exercises frequently applied in muscle-strengthening and therapeutic exercises. The loading devices are often used to increase the training intensity. Objective: To determine the effect of loading devices on muscle activation in squat and lunge and to compare the differences in muscle activation between squat and lunge. Design: Cross-sectional cohort. Participants: Nineteen healthy, male, recreationally active individuals without a history of lower limb injury. Interventions: Each participant performed 10 repetitions of a squat under 5 conditions: unloaded, barbell, dumbbell, loaded vest, and kettlebell, and 10 repetitions of a lunge under 4 conditions: unloaded, barbell, dumbbell, and loaded vest. Main Outcome Measures: The electromyography signals of quadriceps, hamstrings, tibialis anterior, gastrocnemius lateralis and medialis were measured. One-way repeated-measure analysis of variance was used to compare the difference among different loading conditions. Paired t test was used to compare the difference between squat and lunge. Results: The muscle activation in the loaded conditions was significantly higher than that in nonloaded conditions in squat and lunge. Compared with the barbell, dumbbell, and loaded vest conditions, the semitendinosus showed significantly higher activation, and the tibialis anterior showed significantly lower activation in kettlebell condition in squat. No significant difference in muscle activation was found among barbell, dumbbell, and kettlebell conditions in lunge. In addition, quadriceps and hamstring activities were significantly higher in lunge than in squat. Conclusions: Muscle activation was affected by the loading devices in squat but not affected in lunge. Kettlebell squat could be suggested for targeting in strengthening medial hamstring. Progressive strengthening exercise could be recommended from squat to lunge based on sequential activation level. [ABSTRACT FROM AUTHOR]

Published
2020
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37. Ectopic ATP synthase stimulates the secretion of extracellular vesicles in cancer cells.

Author

Kao, Yi-Chun, Chang, Yi-Wen, Lai, Charles P., Chang, Nai-Wen, Huang, Chen-Hao, Chen, Chien-Sheng, Huang, Hsuan-Cheng, and Juan, Hsueh-Fen

Subjects
*ADENOSINE triphosphatase, *EXTRACELLULAR vesicles, *CANCER cells, *PURINERGIC receptors, *SECRETION, *CELL membranes, *FUNGAL cell walls
Abstract

Abstarct: Ectopic ATP synthase on the plasma membrane (eATP synthase) has been found in various cancer types and is a potential target for cancer therapy. However, whether it provides a functional role in tumor progression remains unclear. Here, quantitative proteomics reveals that cancer cells under starvation stress express higher eATP synthase and enhance the production of extracellular vesicles (EVs), which are vital regulators within the tumor microenvironment. Further results show that eATP synthase generates extracellular ATP to stimulate EV secretion by enhancing P2X7 receptor–triggered Ca2+ influx. Surprisingly, eATP synthase is also located on the surface of tumor-secreted EVs. The EVs-surface eATP synthase increases the uptake of tumor-secreted EVs in Jurkat T-cells via association with Fyn, a plasma membrane protein found in immune cells. The eATP synthase-coated EVs uptake subsequently represses the proliferation and cytokine secretion of Jurkat T-cells. This study clarifies the role of eATP synthase on EV secretion and its influence on immune cells. eATP synthase is expressed on the surface of cancer-derived extracellular vesicles (EVs), contributes to EV uptake and reduces Jurkat T cell proliferation and cytokine release. [ABSTRACT FROM AUTHOR]

Published
2023
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