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2. A molecular switch for neuroprotective astrocyte reactivity

Author

Cameron, Evan G., Nahmou, Michael, Toth, Anna B., Heo, Lyong, Tanasa, Bogdan, Dalal, Roopa, Yan, Wenjun, Nallagatla, Pratima, Xia, Xin, Hay, Sarah, Knasel, Cara, Stiles, Travis L., Douglas, Christopher, Atkins, Melissa, Sun, Catalina, Ashouri, Masoumeh, Bian, Minjuan, Chang, Kun-Che, Russano, Kristina, Shah, Sahil, Woodworth, Mollie B., Galvao, Joana, Nair, Ramesh V., Kapiloff, Michael S., and Goldberg, Jeffrey L.

Published
2024
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9. NF1 mutation drives neuronal activity-dependent initiation of optic glioma

Author

Pan, Yuan, Hysinger, Jared D, Barron, Tara, Schindler, Nicki F, Cobb, Olivia, Guo, Xiaofan, Yalçın, Belgin, Anastasaki, Corina, Mulinyawe, Sara B, Ponnuswami, Anitha, Scheaffer, Suzanne, Ma, Yu, Chang, Kun-Che, Xia, Xin, Toonen, Joseph A, Lennon, James J, Gibson, Erin M, Huguenard, John R, Liau, Linda M, Goldberg, Jeffrey L, Monje, Michelle, and Gutmann, David H

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Neurofibromatosis, Brain Disorders, Rare Diseases, Cancer, Stem Cell Research - Nonembryonic - Non-Human, Genetics, Eye Disease and Disorders of Vision, Stem Cell Research, Neurosciences, 2.1 Biological and endogenous factors, Aetiology, Neurological, Animals, Astrocytoma, Cell Adhesion Molecules, Neuronal, Cell Transformation, Neoplastic, Female, Genes, Neurofibromatosis 1, Germ-Line Mutation, Humans, Male, Membrane Proteins, Mice, Mutation, Nerve Tissue Proteins, Neurofibromin 1, Neurons, Optic Nerve, Optic Nerve Glioma, Photic Stimulation, Retina, General Science & Technology
Abstract

Neurons have recently emerged as essential cellular constituents of the tumour microenvironment, and their activity has been shown to increase the growth of a diverse number of solid tumours1. Although the role of neurons in tumour progression has previously been demonstrated2, the importance of neuronal activity to tumour initiation is less clear-particularly in the setting of cancer predisposition syndromes. Fifteen per cent of individuals with the neurofibromatosis 1 (NF1) cancer predisposition syndrome (in which tumours arise in close association with nerves) develop low-grade neoplasms of the optic pathway (known as optic pathway gliomas (OPGs)) during early childhood3,4, raising  the possibility that postnatal light-induced activity of the optic nerve drives tumour initiation. Here we use an authenticated mouse model of OPG driven by mutations in the neurofibromatosis 1 tumour suppressor gene (Nf1)5 to demonstrate that stimulation of optic nerve activity increases optic glioma growth, and that decreasing visual experience via light deprivation prevents tumour formation and maintenance. We show that the initiation of Nf1-driven OPGs (Nf1-OPGs) depends on visual experience during a developmental period in which Nf1-mutant mice are susceptible to tumorigenesis. Germline Nf1 mutation in retinal neurons results in aberrantly increased shedding of neuroligin 3 (NLGN3) within the optic nerve in response to retinal neuronal activity. Moreover, genetic Nlgn3 loss or pharmacological inhibition of NLGN3 shedding blocks the formation and progression of Nf1-OPGs. Collectively, our studies establish an obligate role for neuronal activity in the development of some types of brain tumours, elucidate a therapeutic strategy to reduce OPG incidence or mitigate tumour progression, and underscore the role of Nf1mutation-mediated dysregulation of neuronal signalling pathways in mouse models of the NF1 cancer predisposition syndrome.

Published
2021

14. A molecular switch for neuroprotective astrocyte reactivity

Author

Cameron, Evan G., primary, Nahmou, Michael, additional, Toth, Anna B., additional, Heo, Lyong, additional, Tanasa, Bogdan, additional, Dalal, Roopa, additional, Yan, Wenjun, additional, Nallagatla, Pratima, additional, Xia, Xin, additional, Hay, Sarah, additional, Knasel, Cara, additional, Stiles, Travis L., additional, Douglas, Christopher, additional, Atkins, Melissa, additional, Sun, Catalina, additional, Ashouri, Masoumeh, additional, Bian, Minjuan, additional, Chang, Kun-Che, additional, Russano, Kristina, additional, Shah, Sahil, additional, Woodworth, Mollie B., additional, Galvao, Joana, additional, Nair, Ramesh V., additional, Kapiloff, Michael S., additional, and Goldberg, Jeffrey L., additional

Published
2023
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16. Contributors

Author

Anderson, Graham, primary, Bagnaninchi, Pierre, additional, Baumel, Bernard, additional, Birbrair, Alexander, additional, Bloomquist, Ryan, additional, Bugallo-Casal, Ana, additional, Camargo, Christian, additional, Campos, Francisco, additional, Chang, Kun-Che, additional, Cheema, Umber, additional, Dardik, Alan, additional, Das, Jugal Kishore, additional, Dhillon, Baljean, additional, Donato, M. Teresa, additional, Dunbar, G.L., additional, Gao, Xixiang, additional, Gorecka, Jolanta, additional, Gu, Yongquan, additional, Khoo, Chin Meng, additional, Kim, Kwang-Soo, additional, Kumar, Anil, additional, Lau, Hwee Hui, additional, Luo, Ziming, additional, Marrero, Michelle, additional, Miyagawa, Shigeru, additional, Mozaffari, Mahmood S., additional, Nahmou, Michael, additional, Ohyama, Manabu, additional, Parraguez, Víctor H., additional, Pelechá, María, additional, Peng, Hao-Yun, additional, Peralta, Oscar A., additional, Pinto, Milena, additional, Pérez-Mato, María, additional, Ren, Yijie, additional, Rossignol, J., additional, Sawa, Yoshiki, additional, Schweitzer, Jeffrey S., additional, Song, Bin, additional, Song, Jianxun, additional, Srinageshwar, B., additional, Tan, Wei Xuan, additional, Tan, Nguan Soon, additional, Teo, Adrian Kee Keong, additional, Tolosa, Laia, additional, Torres, Cristian G., additional, Wang, Liqing, additional, Wu, Yingfeng, additional, and Xiong, Xiaofang, additional

Published
2021
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20. Nordalbergin Exerts Anti-Neuroinflammatory Effects by Attenuating MAPK Signaling Pathway, NLRP3 Inflammasome Activation and ROS Production in LPS-Stimulated BV2 Microglia

Author

Lo, Jung, primary, Wu, Hsin-En, additional, Liu, Ching-Chih, additional, Chang, Kun-Che, additional, Lee, Po-Yen, additional, Liu, Po-Len, additional, Huang, Shu-Pin, additional, Wu, Pei-Chang, additional, Lin, Tzu-Chieh, additional, Lai, Yu-Hung, additional, Chang, Yo-Chen, additional, Chen, Yuan-Ru, additional, Lee, Sheng-I, additional, Huang, Yu-Kai, additional, Wang, Shu-Chi, additional, and Li, Chia-Yang, additional

Published
2023
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23. Directly induced human retinal ganglion cells mimic fetal RGCs and are neuroprotective after transplantation in vivo

Author

Luo, Ziming, primary, Chang, Kun-Che, additional, Wu, Suqian, additional, Sun, Catalina, additional, Xia, Xin, additional, Nahmou, Michael, additional, Bian, Minjuan, additional, Wen, Rain R., additional, Zhu, Ying, additional, Shah, Sahil, additional, Tanasa, Bogdan, additional, Wernig, Marius, additional, and Goldberg, Jeffrey L., additional

Published
2022
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27. TAMI-69. NF1 MUTATION DRIVES NEURONAL ACTIVITY-DEPENDENT OPTIC GLIOMA INITIATION

Author

Pan, Yuan, primary, Hysinger, Jared, additional, Barron, Tara, additional, Schindler, Nicki, additional, Cobb, Olivia, additional, Guo, Xiaofan, additional, Yalçın, Belgin, additional, Anastasaki, Corina, additional, Mulinyawe, Sara, additional, Ponnuswami, Anitha, additional, Scheaffer, Suzanne, additional, Ma, Yu, additional, Chang, Kun-Che, additional, Xia, Xin, additional, Toonen, Joseph, additional, Lennon, James, additional, Gibson, Erin, additional, Huguenard, John, additional, Liau, Linda, additional, Goldberg, Jeffrey, additional, Monje, Michelle, additional, and Gutmann, David, additional

Published
2021
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28. LGG-01. NF1 MUTATION DRIVES NEURONAL ACTIVITY-DEPENDENT OPTIC GLIOMA INITIATION

Author

Pan, Yuan, primary, Hysinger, Jared, additional, Schindler, Nicki, additional, Cobb, Olivia, additional, Guo, Xiaofan, additional, Yalçın, Belgin, additional, Anastasaki, Corina, additional, Mulinyawe, Sara, additional, Ponnuswami, Anitha, additional, Scheaffer, Suzanne, additional, Ma, Yu, additional, Chang, Kun-Che, additional, Xia, Xin, additional, Toonen, Joseph, additional, Lennon, James, additional, Gibson, Erin, additional, Liau, Linda, additional, Goldberg, Jeffrey, additional, Monje, Michelle, additional, and Gutmann, David, additional

Published
2021
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30. Posttranslational Modification of Sox11 Regulates RGC Survival and Axon Regeneration

Author

Chang, Kun-Che, primary, Bian, Minjuan, additional, Xia, Xin, additional, Madaan, Ankush, additional, Sun, Catalina, additional, Wang, Qizhao, additional, Li, Liang, additional, Nahmou, Michael, additional, Noro, Takahiko, additional, Yokota, Satoshi, additional, Galvao, Joana, additional, Kreymerman, Alexander, additional, Tanasa, Bogdan, additional, Hu, Yang, additional, and Goldberg, Jeffrey L., additional

Published
2021
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31. MEF2 transcription factors differentially contribute to retinal ganglion cell loss after optic nerve injury

Author

Xia, Xin, primary, Yu, Caroline Y., additional, Bian, Minjuan, additional, Sun, Catalina B., additional, Tanasa, Bogdan, additional, Chang, Kun-Che, additional, Bruffett, Dawn M., additional, Thakur, Hrishikesh, additional, Shah, Sahil H., additional, Knasel, Cara, additional, Cameron, Evan G., additional, Kapiloff, Michael S., additional, and Goldberg, Jeffrey L., additional

Published
2020
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32. Defective INPP5E distribution in NPHP1‐related Senior–Loken syndrome

Author

Ning, Ke, primary, Song, Emilie, additional, Sendayen, Brent E., additional, Prosseda, Philipp P., additional, Chang, Kun‐Che, additional, Ghaffarieh, Alireza, additional, Alvarado, Jorge A., additional, Wang, Biao, additional, Haider, Kathryn M., additional, Berbari, Nicolas F., additional, Hu, Yang, additional, and Sun, Yang, additional

Published
2020
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35. Cell transplantation of retinal ganglion cells derived from hESCs

Author

Zhang, Xiong, primary, Tenerelli, Kevin, additional, Wu, Suqian, additional, Xia, Xin, additional, Yokota, Satoshi, additional, Sun, Catalina, additional, Galvao, Joana, additional, Venugopalan, Praseeda, additional, Li, Chenyi, additional, Madaan, Ankush, additional, Goldberg, Jeffrey L., additional, and Chang, Kun-Che, additional

Published
2020
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36. Mouse γ-Synuclein Promoter-Mediated Gene Expression and Editing in Mammalian Retinal Ganglion Cells

Author

Wang, Qizhao, primary, Zhuang, Pei, additional, Huang, Haoliang, additional, Li, Liang, additional, Liu, Liang, additional, Webber, Hannah C., additional, Dalal, Roopa, additional, Siew, Leonard, additional, Fligor, Clarisse M., additional, Chang, Kun-Che, additional, Nahmou, Michael, additional, Kreymerman, Alexander, additional, Sun, Yang, additional, Meyer, Jason S., additional, Goldberg, Jeffrey Louis, additional, and Hu, Yang, additional

Published
2020
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38. Opposing Effects of Growth and Differentiation Factors in Cell-Fate Specification

Author

Chang, Kun-Che, primary, Sun, Catalina, additional, Cameron, Evan G., additional, Madaan, Ankush, additional, Wu, Suqian, additional, Xia, Xin, additional, Zhang, Xiong, additional, Tenerelli, Kevin, additional, Nahmou, Michael, additional, Knasel, Cara M., additional, Russano, Kristina R., additional, Hertz, Jonathan, additional, and Goldberg, Jeffrey L., additional

Published
2019
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40. TNF-α Mediates Eosinophil Cationic Protein-induced Apoptosis in BEAS-2B Cells

Author

Chao Chih-Chung, Fang Shun-lung, Chung Cheng-Ta, Chang Chuan-Hsin, Shu Chih-Wen, Chang Margaret, Fan Tan-chi, Lo Chih-Wei, Chang Kun-Che, Tsai Jaw-Ji, and Lai Yiu-Kay

Subjects
Cytology, QH573-671
Abstract

Abstract Background Eosinophilic granulocytes are important for the human immune system. Many cationic proteins with cytotoxic activities, such as eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN), are released from activated eosinophils. ECP, with low RNase activity, is widely used as a biomarker for asthma. ECP inhibits cell viability and induces apoptosis to cells. However, the specific pathway underlying the mechanisms of ECP-induced cytotoxicity remains unclear. This study investigated ECP-induced apoptosis in bronchial epithelial BEAS-2B cells and elucidated the specific pathway during apoptosis. Results To address the mechanisms involved in ECP-induced apoptosis in human BEAS-2B cells, investigation was carried out using chromatin condensation, cleavage of poly (ADP-ribose) polymerase (PARP), sub-G1 distribution in cell cycle, annexin V labeling, and general or specific caspase inhibitors. Caspase-8-dependent apoptosis was demonstrated by cleavage of caspase-8 after recombinant ECP treatment, accompanied with elevated level of tumor necrosis factor alpha (TNF-α). Moreover, ECP-induced apoptosis was effectively inhibited in the presence of neutralizing anti-TNF-α antibody. Conclusion In conclusion, our results have demonstrated that ECP increased TNF-α production in BEAS-2B cells and triggered apoptosis by caspase-8 activation through mitochondria-independent pathway.

Published
2010
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41. Defective INPP5E distribution in NPHP1‐related Senior–Loken syndrome.

Author

Ning, Ke, Song, Emilie, Sendayen, Brent E., Prosseda, Philipp P., Chang, Kun‐Che, Ghaffarieh, Alireza, Alvarado, Jorge A., Wang, Biao, Haider, Kathryn M., Berbari, Nicolas F., Hu, Yang, and Sun, Yang

Subjects
CILIA & ciliary motion, CYSTIC kidney disease, KIDNEY tubules, CHRONIC kidney failure, KIDNEY physiology, RETINAL degeneration, CILIOPATHY
Abstract

Background: Senior–Loken syndrome is a rare genetic disorder that presents with nephronophthisis and retinal degeneration, leading to end‐stage renal disease and progressive blindness. The most frequent cause of juvenile nephronophthisis is a mutation in the nephronophthisis type 1 (NPHP1) gene. NPHP1 encodes the protein nephrocystin‐1, which functions at the transition zone (TZ) of primary cilia. Methods: We report a 9‐year‐old Senior–Loken syndrome boy with NPHP1 deletion, who presents with bilateral vision decrease and cystic renal disease. Renal function deteriorated to require bilateral nephrectomy and renal transplant. We performed immunohistochemistry, H&E staining, and electron microscopy on the renal sample to determine the subcellular distribution of ciliary proteins in the absence of NPHP1. Results: Immunohistochemistry and electron microscopy of the resected kidney showed disorganized cystic structures with loss of cilia in renal tubules. Phosphoinositides have been recently recognized as critical components of the ciliary membrane and immunostaining of kidney sections for phosphoinositide 5‐phosphatase, INPP5E, showed loss of staining compared to healthy control. Ophthalmic examination showed decreased electroretinogram consistent with early retinal degeneration. Conclusion: The decreased expression of INPP5E specifically in the primary cilium, coupled with disorganized cilia morphology, suggests a novel role of NPHP1 that it is involved in regulating ciliary phosphoinositide composition in the ciliary membrane of renal tubular cells. In this study, we report a 9‐year‐old Senior‐Loken syndrome patient with NPHP1 deletion. We found the decreased expression of INPP5E specifically in the primary cilium, coupled with disorganized cilia morphology, suggests a novel role of NPHP1 in regulating ciliary phosphoinositide composition in the ciliary membrane of renal tubular cells. [ABSTRACT FROM AUTHOR]

Published
2021
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45. NF1mutation drives neuronal activity-dependent initiation of optic glioma

Author

Pan, Yuan, Hysinger, Jared D., Barron, Tara, Schindler, Nicki F., Cobb, Olivia, Guo, Xiaofan, Yalçın, Belgin, Anastasaki, Corina, Mulinyawe, Sara B., Ponnuswami, Anitha, Scheaffer, Suzanne, Ma, Yu, Chang, Kun-Che, Xia, Xin, Toonen, Joseph A., Lennon, James J., Gibson, Erin M., Huguenard, John R., Liau, Linda M., Goldberg, Jeffrey L., Monje, Michelle, and Gutmann, David H.

Abstract

Neurons have recently emerged as essential cellular constituents of the tumour microenvironment, and their activity has been shown to increase the growth of a diverse number of solid tumours1. Although the role of neurons in tumour progression has previously been demonstrated2, the importance of neuronal activity to tumour initiation is less clear—particularly in the setting of cancer predisposition syndromes. Fifteen per cent of individuals with the neurofibromatosis 1 (NF1) cancer predisposition syndrome (in which tumours arise in close association with nerves) develop low-grade neoplasms of the optic pathway (known as optic pathway gliomas (OPGs)) during early childhood3,4, raising  the possibility that postnatal light-induced activity of the optic nerve drives tumour initiation. Here we use an authenticated mouse model of OPG driven by mutations in the neurofibromatosis 1 tumour suppressor gene (Nf1)5to demonstrate that stimulation of optic nerve activity increases optic glioma growth, and that decreasing visual experience via light deprivation prevents tumour formation and maintenance. We show that the initiation of Nf1-driven OPGs (Nf1-OPGs) depends on visual experience during a developmental period in which Nf1-mutant mice are susceptible to tumorigenesis. Germline Nf1mutation in retinal neurons results in aberrantly increased shedding of neuroligin 3 (NLGN3) within the optic nerve in response to retinal neuronal activity. Moreover, genetic Nlgn3loss or pharmacological inhibition of NLGN3 shedding blocks the formation and progression of Nf1-OPGs. Collectively, our studies establish an obligate role for neuronal activity in the development of some types of brain tumours, elucidate a therapeutic strategy to reduce OPG incidence or mitigate tumour progression, and underscore the role of Nf1mutation-mediated dysregulation of neuronal signalling pathways in mouse models of the NF1 cancer predisposition syndrome.

Published
2021
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46. Novel Regulatory Mechanisms for the SoxC Transcriptional Network Required for Visual Pathway Development

Author

Chang, Kun-Che, primary, Hertz, Jonathan, additional, Zhang, Xiong, additional, Jin, Xiao-Lu, additional, Shaw, Peter, additional, Derosa, Brooke A., additional, Li, Janet Y., additional, Venugopalan, Praseeda, additional, Valenzuela, Daniel A., additional, Patel, Roshni D., additional, Russano, Kristina R., additional, Alshamekh, Shomoukh A., additional, Sun, Catalina, additional, Tenerelli, Kevin, additional, Li, Chenyi, additional, Velmeshev, Dmitri, additional, Cheng, Yuyan, additional, Boyce, Timothy M., additional, Dreyfuss, Alexandra, additional, Uddin, Mohammed S., additional, Muller, Kenneth J., additional, Dykxhoorn, Derek M., additional, and Goldberg, Jeffrey L., additional

Published
2017
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