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19 results on '"Bian, Minjuan"'

1. 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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2. Ca2+/Calmodulin-Dependent Protein Kinase II Enhances Retinal Ganglion Cell Survival But Suppresses Axon Regeneration after Optic Nerve Injury

Author

Xia, Xin, primary, Shi, Caleb, additional, Tsien, Christina, additional, Sun, Catalina B., additional, Xie, Lili, additional, Luo, Ziming, additional, Bian, Minjuan, additional, Russano, Kristina, additional, Thakur, Hrishikesh Singh, additional, Benowitz, Larry I., additional, Goldberg, Jeffrey L., additional, and Kapiloff, Michael S., additional

Published
2024
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3. 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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4. 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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8. 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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9. 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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10. Combination of ginsenoside Rb1 and Rd protects the retina against bright light-induced degeneration

Author

Teng Zhang, Xiaoye Du, Jing Xu, Yu Chen, Jingang Cui, Bian Minjuan, Peiwei Wang, and Jiangping Gu

Subjects
0301 basic medicine, Retinal degeneration, Ginsenosides, Light, Science, Gene Expression, Pharmacology, Protective Agents, medicine.disease_cause, Antioxidants, Retina, Article, Proinflammatory cytokine, Mice, 03 medical and health sciences, chemistry.chemical_compound, Gene expression, Cell Adhesion, Animals, Medicine, Photoreceptor Cells, Mice, Inbred BALB C, Multidisciplinary, Microglia, business.industry, Retinal Degeneration, Retinal, Saponins, medicine.disease, eye diseases, Oxidative Stress, RAW 264.7 Cells, 030104 developmental biology, medicine.anatomical_structure, chemistry, Neuroglia, sense organs, Inflammation Mediators, Reactive Oxygen Species, business, Biomarkers, Oxidative stress
Abstract

Photoreceptor degeneration is a central pathology of various retinal degenerative diseases which currently lack effective therapies. Antioxidant and anti-inflammatory activities are noted for Panax notoginsenoside saponins (PNS) and related saponin compound(s). However, the photoreceptor protective potentials of PNS or related saponin compound(s) remain unknown. The current study revealed that PNS protected against photoreceptor loss in bright light-exposed BALB/c mice. Combination of ginsenoside Rb1 and Rd, two major saponin compounds of PNS, recapitulated the retinal protection of PNS and attenuated retinal oxidative stress and inflammatory changes. Rb1 or Rd partially alleviated all-trans-Retinal-induced oxidative stress in ARPE19 cells. Rb1 or Rd suppressed lipopolysaccharides (LPS)-induced proinflammatory gene expression in ARPE19 and RAW264.7 cells. Rb1 or Rd also modulated the expression of proinflammatory microRNA, miR-155 and its direct target, anti-inflammatory SHIP1, in LPS-stimulated RAW264.7 cells. The retinal expression of miR-155 and SHIP1 was altered preceding extensive retinal damage, which was maintained at normal level by Rb1 and Rd combination. This work shows for the first time that altered expression of miR-155 and SHIP1 are involved in photoreceptor degeneration. Most importantly, novel retinal protective activities of combination of Rb1 and Rd justify further evaluation for the treatment of related retinal degenerative disorders.

Published
2017

14. Celastrol protects mouse retinas from bright light-induced degeneration through inhibition of oxidative stress and inflammation.

Author

Minjuan Bian, Xiaoye Du, Jingang Cui, Peiwei Wang, Wenjian Wang, Weiliang Zhu, Teng Zhang, Yu Chen, Bian, Minjuan, Du, Xiaoye, Cui, Jingang, Wang, Peiwei, Wang, Wenjian, Zhu, Weiliang, Zhang, Teng, and Chen, Yu

Subjects
RETINAL degeneration treatment, PHOTORECEPTORS, OXIDATIVE stress, CELL death inhibition, LABORATORY mice, THERAPEUTIC use of cytokines, PHOTOTHERAPY, INFLAMMATION prevention, HYDROCARBON metabolism, ANIMALS, BIOLOGICAL models, CELL culture, CELL receptors, CYTOKINES, CYTOSKELETAL proteins, DOSE-effect relationship in pharmacology, GENES, HYDROCARBONS, INFLAMMATION, LIGHT, DOSE-response relationship (Radiation), MICE, RETINAL diseases, NEUROPROTECTIVE agents, LIPOPOLYSACCHARIDES, PHARMACODYNAMICS, PHYSIOLOGICAL effects of radiation, PREVENTION, THERAPEUTICS
Abstract

Background: Photoreceptor death leads to vision impairment in several retinal degenerative disorders. Therapies protecting photoreceptor from degeneration remain to be developed. Anti-inflammation, anti-oxidative stress, and neuroprotective effects of celastrol have been demonstrated in a variety of disease models. The current study aimed to investigate the photoreceptor protective effect of celastrol.Methods: Bright light-induced retinal degeneration in BALB/c mice was used, and morphological, functional, and molecular changes of retina were evaluated in the absence and presence of celastrol treatment.Results: Significant morphological and functional protection was observed as a result of celastrol treatment in bright light-exposed BALB/c mice. Celastrol treatment resulted in suppression of cell death in photoreceptor cells, alleviation of oxidative stress in the retinal pigment epithelium and photoreceptors, downregulation of retinal expression of proinflammatory genes, and suppression of microglia activation and gliosis in the retina. Additionally, leukostasis was found to be induced in the retinal vasculature in light-exposed BALB/c mice, which was significantly attenuated by celastrol treatment. In vitro, celastrol attenuated all-trans-retinal-induced oxidative stress in cultured APRE19 cells. Moreover, celastrol treatment significantly suppressed lipopolysaccharides-stimulated expression of proinflammatory genes in both APRE19 and RAW264.7 cells.Conclusions: The results demonstrated for the first time that celastrol prevents against light-induced retinal degeneration through inhibition of retinal oxidative stress and inflammation. [ABSTRACT FROM AUTHOR]

Published
2016
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18. Celastrol protects mouse retinas from bright light-induced degeneration through inhibition of oxidative stress and inflammation

Author

Teng Zhang, Xiaoye Du, Zhu Weiliang, Wenjian Wang, Bian Minjuan, Yu Chen, Peiwei Wang, and Jingang Cui

Subjects
Lipopolysaccharides, 0301 basic medicine, Retinal degeneration, Opsin, Light, genetic structures, Degeneration (medical), medicine.disease_cause, Mice, chemistry.chemical_compound, 0302 clinical medicine, Cells, Cultured, Mice, Inbred BALB C, General Neuroscience, Retinal Degeneration, Cell biology, Neuroprotective Agents, Neurology, Celastrol, Cytokines, Female, medicine.symptom, Pentacyclic Triterpenes, Rhodopsin, Immunology, Inflammation, Neuroprotection, 03 medical and health sciences, Cellular and Molecular Neuroscience, Glial Fibrillary Acidic Protein, medicine, Animals, Dose-Response Relationship, Drug, Opsins, business.industry, Research, Dose-Response Relationship, Radiation, Retinal, medicine.disease, Triterpenes, eye diseases, Disease Models, Animal, Oxidative Stress, 030104 developmental biology, Gene Expression Regulation, chemistry, sense organs, business, Neuroscience, 030217 neurology & neurosurgery, Oxidative stress
Abstract

Background Photoreceptor death leads to vision impairment in several retinal degenerative disorders. Therapies protecting photoreceptor from degeneration remain to be developed. Anti-inflammation, anti-oxidative stress, and neuroprotective effects of celastrol have been demonstrated in a variety of disease models. The current study aimed to investigate the photoreceptor protective effect of celastrol. Methods Bright light-induced retinal degeneration in BALB/c mice was used, and morphological, functional, and molecular changes of retina were evaluated in the absence and presence of celastrol treatment. Results Significant morphological and functional protection was observed as a result of celastrol treatment in bright light-exposed BALB/c mice. Celastrol treatment resulted in suppression of cell death in photoreceptor cells, alleviation of oxidative stress in the retinal pigment epithelium and photoreceptors, downregulation of retinal expression of proinflammatory genes, and suppression of microglia activation and gliosis in the retina. Additionally, leukostasis was found to be induced in the retinal vasculature in light-exposed BALB/c mice, which was significantly attenuated by celastrol treatment. In vitro, celastrol attenuated all-trans-retinal-induced oxidative stress in cultured APRE19 cells. Moreover, celastrol treatment significantly suppressed lipopolysaccharides-stimulated expression of proinflammatory genes in both APRE19 and RAW264.7 cells. Conclusions The results demonstrated for the first time that celastrol prevents against light-induced retinal degeneration through inhibition of retinal oxidative stress and inflammation. Electronic supplementary material The online version of this article (doi:10.1186/s12974-016-0516-8) contains supplementary material, which is available to authorized users.

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19. Ca 2+ /Calmodulin-Dependent Protein Kinase II Enhances Retinal Ganglion Cell Survival But Suppresses Axon Regeneration after Optic Nerve Injury.

Author

Xia X, Shi C, Tsien C, Sun CB, Xie L, Luo Z, Bian M, Russano K, Thakur HS, Benowitz LI, Goldberg JL, and Kapiloff MS

Subjects
Mice, Animals, Retinal Ganglion Cells metabolism, Calcium-Calmodulin-Dependent Protein Kinase Type 2 metabolism, Axons metabolism, Nerve Regeneration physiology, Protein Isoforms metabolism, Cell Survival physiology, Optic Nerve Injuries metabolism, Neurodegenerative Diseases metabolism, Optic Nerve Diseases metabolism
Abstract

Neuroprotection after injury or in neurodegenerative disease remains a major goal for basic and translational neuroscience. Retinal ganglion cells (RGCs), the projection neurons of the eye, degenerate in optic neuropathies after axon injury, and there are no clinical therapies to prevent their loss or restore their connectivity to targets in the brain. Here we demonstrate a profound neuroprotective effect of the exogenous expression of various Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) isoforms in mice. A dramatic increase in RGC survival following the optic nerve trauma was elicited by the expression of constitutively active variants of multiple CaMKII isoforms in RGCs using adeno-associated viral (AAV) vectors across a 100-fold range of AAV dosing in vivo. Despite this neuroprotection, however, short-distance RGC axon sprouting was suppressed by CaMKII, and long-distance axon regeneration elicited by several pro-axon growth treatments was likewise inhibited even as CaMKII further enhanced RGC survival. Notably, in a dose-escalation study, AAV-expressed CaMKII was more potent for axon growth suppression than the promotion of survival. That diffuse overexpression of constitutively active CaMKII strongly promotes RGC survival after axon injury may be clinically valuable for neuroprotection per se. However, the associated strong suppression of the optic nerve axon regeneration demonstrates the need for understanding the intracellular domain- and target-specific CaMKII activities to the development of CaMKII signaling pathway-directed strategies for the treatment of optic neuropathies., Competing Interests: The authors declare no competing financial interests., (Copyright © 2024 Xia et al.)

Published
2024
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