Neural Regeneration Research最新文献

Neuropeptide cholecystokinin: a key neuromodulator for hippocampal functions 神经肽胆囊收缩素：海马功能的关键神经调节剂

Neural Regeneration Research Pub Date : 2024-07-10 DOI: 10.4103/nrr.nrr-d-24-00465

Fengwen Huang, Stephen Temitayo Bello

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Calcium-sensitive protein MLC1 as a possible modulator of the astrocyte functional state 钙敏感蛋白 MLC1 可能是星形胶质细胞功能状态的调节器

Neural Regeneration Research Pub Date : 2024-07-10 DOI: 10.4103/nrr.nrr-d-24-00471

E. Ambrosini, A. Lanciotti, M. S. Brignone

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Neuroinflammation revisited through the microglial lens 通过小胶质细胞透镜重新审视神经炎症

Neural Regeneration Research Pub Date : 2024-07-10 DOI: 10.4103/nrr.nrr-d-24-00284

R. Socodato, João B. Relvas

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New insights on the role of chondroitin sulfate proteoglycans in neural stem cell–mediated repair in spinal cord injury 硫酸软骨素蛋白多糖在神经干细胞介导的脊髓损伤修复中的作用新见解

Neural Regeneration Research Pub Date : 2024-07-10 DOI: 10.4103/nrr.nrr-d-24-00378

Seyed Mojtaba Hosseini, Soheila Karimi-Abdolrezaee

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Data-driven drug repositioning using olfactory omics profiles: challenges and perspectives in neurodegeneration 利用嗅觉 omics 图谱进行数据驱动的药物重新定位：神经退行性疾病的挑战与前景

Neural Regeneration Research Pub Date : 2024-07-10 DOI: 10.4103/nrr.nrr-d-24-00334

P. Cartas-Cejudo, Adriana Cortés, Mercedes Lachén-Montes, Elena Anaya-Cubero, Joaquín Fernández-Irigoyen, E. Santamaría

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PGLYRP1 protein as a novel mediator of cellular dialogue in neuroinflammation PGLYRP1 蛋白是神经炎症中细胞对话的新型介质

Neural Regeneration Research Pub Date : 2024-07-10 DOI: 10.4103/nrr.nrr-d-24-00424

Anup Bhusal, Won-Ha Lee, K. Suk

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Sleep as a window to understand and regulate Alzheimer’s disease: emerging roles of thalamic reticular nucleus 睡眠是了解和调节阿尔茨海默病的窗口：丘脑网状核的新作用

Neural Regeneration Research Pub Date : 2024-07-10 DOI: 10.4103/nrr.nrr-d-24-00351

Haoqi Sun, Shiqian Shen, Robert J. Thomas, M. Westover, Can Zhang

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Na+/K+-ATPase: ion pump, signal transducer, or cytoprotective protein, and novel biological functions Na+/K+-ATP 酶：离子泵、信号转换器或细胞保护蛋白，以及新的生物功能

Neural Regeneration Research Pub Date : 2024-01-31 DOI: 10.4103/nrr.nrr-d-23-01175

Songqiang Huang, Wanting Dong, Xiaoqian Lin, Jin-Song Bian

{"title":"Na+/K+-ATPase: ion pump, signal transducer, or cytoprotective protein, and novel biological functions","authors":"Songqiang Huang, Wanting Dong, Xiaoqian Lin, Jin-Song Bian","doi":"10.4103/nrr.nrr-d-23-01175","DOIUrl":"https://doi.org/10.4103/nrr.nrr-d-23-01175","url":null,"abstract":"\u0000 Na+/K+-ATPase is a transmembrane protein that has important roles in the maintenance of electrochemical gradients across cell membranes by transporting three Na+ out of and two K+ into cells. Additionally, Na+/K+-ATPase participates in Ca2+-signaling transduction and neurotransmitter release by coordinating the ion concentration gradient across the cell membrane. Na+/K+-ATPase works synergistically with multiple ion channels in the cell membrane to form a dynamic network of ion homeostatic regulation and affects cellular communication by regulating chemical signals and the ion balance among different types of cells. Therefore, it is not surprising that Na+/K+-ATPase dysfunction has emerged as a risk factor for a variety of neurological diseases. However, published studies have so far only elucidated the important roles of Na+/K+-ATPase dysfunction in disease development, and we are lacking detailed mechanisms to clarify how Na+/K+-ATPase affects cell function. Our recent studies revealed that membrane loss of Na+/K+-ATPase is a key mechanism in many neurological disorders, particularly stroke and Parkinson’s disease. Stabilization of plasma membrane Na+/K+-ATPase with an antibody is a novel strategy to treat these diseases. For this reason, Na+/K+-ATPase acts not only as a simple ion pump but also as a sensor/ regulator or cytoprotective protein, participating in signal transduction such as neuronal autophagy and apoptosis, glial cell migration, etc. Thus, the present review attempts to summarize the novel biological functions of Na+/K+-ATPase and Na+/K+-ATPase-related pathogenesis. The potential for novel strategies to treat Na+/K+-ATPase-related brain diseases will also be discussed.","PeriodicalId":506566,"journal":{"name":"Neural Regeneration Research","volume":"165 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140477309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Small extracellular vesicles derived from human induced pluripotent stem cell-differentiated neural progenitor cells mitigate retinal ganglion cell degeneration in a mouse model of optic nerve injury 在小鼠视神经损伤模型中，由诱导多能干细胞分化的神经祖细胞衍生的细胞外小泡可减轻视网膜神经节细胞的退化

Neural Regeneration Research Pub Date : 2024-01-31 DOI: 10.4103/nrr.nrr-d-23-01414

Tong Li, Hui-Min Xing, Hai-Dong Qian, Qiao Gao, Shenglan Xu, Hua Ma, Zai-Long Chi

{"title":"Small extracellular vesicles derived from human induced pluripotent stem cell-differentiated neural progenitor cells mitigate retinal ganglion cell degeneration in a mouse model of optic nerve injury","authors":"Tong Li, Hui-Min Xing, Hai-Dong Qian, Qiao Gao, Shenglan Xu, Hua Ma, Zai-Long Chi","doi":"10.4103/nrr.nrr-d-23-01414","DOIUrl":"https://doi.org/10.4103/nrr.nrr-d-23-01414","url":null,"abstract":"\u0000 Several studies have found that transplantation of neural progenitor cells (NPCs) promotes the survival of injured neurons. However, a poor integration rate and high risk of tumorigenicity after cell transplantation limits their clinical application. Small extracellular vesicles (sEVs) contain bioactive molecules for neuronal protection and regeneration. Previous studies have shown that stem/progenitor cell-derived sEVs can promote neuronal survival and recovery of neurological function in neurodegenerative eye diseases and other eye diseases. In this study, we intravitreally transplanted sEVs derived from human induced pluripotent stem cells (hiPSCs) and hiPSCs-differentiated NPCs (hiPSC-NPC) in a mouse model of optic nerve crush. Our results show that these intravitreally injected sEVs were ingested by retinal cells, especially those localized in the ganglion cell layer. Treatment with hiPSC-NPC derived sEVs mitigated optic nerve crush-induced retinal ganglion cell degeneration, and regulated the retinal microenvironment by inhibiting excessive activation of microglia. Component analysis further revealed that hiPSC-NPC derived sEVs transported neuroprotective and anti-inflammatory miRNA cargos to target cells, which had protective effects on RGCs after optic nerve injury. These findings suggest that sEVs derived from hiPSC-NPC are a promising cell-free therapeutic strategy for optic neuropathy.","PeriodicalId":506566,"journal":{"name":"Neural Regeneration Research","volume":"136 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140476112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Endoplasmic reticulum stress and autophagy in cerebral ischemia/reperfusion injury: PERK as a potential target for intervention 脑缺血再灌注损伤中的内质网应激和自噬：作为潜在干预靶点的 PERK

Neural Regeneration Research Pub Date : 2024-01-31 DOI: 10.4103/nrr.nrr-d-23-00794

Ju Zheng, Yixin Li, Ting Zhang, Yanlin Fu, Peiyan Long, Xiao Gao, Zhengwei Wang, Zhizhong Guan, Xiaolan Qi, Wei Hong, Yan Xiao

{"title":"Endoplasmic reticulum stress and autophagy in cerebral ischemia/reperfusion injury: PERK as a potential target for intervention","authors":"Ju Zheng, Yixin Li, Ting Zhang, Yanlin Fu, Peiyan Long, Xiao Gao, Zhengwei Wang, Zhizhong Guan, Xiaolan Qi, Wei Hong, Yan Xiao","doi":"10.4103/nrr.nrr-d-23-00794","DOIUrl":"https://doi.org/10.4103/nrr.nrr-d-23-00794","url":null,"abstract":"\u0000 Several studies have shown that activation of unfolded protein response and endoplasmic reticulum (ER) stress plays a crucial role in severe cerebral ischemia/reperfusion injury. Autophagy occurs within hours after cerebral ischemia, but the relationship between ER stress and autophagy remains unclear. In this study, we established experimental models using oxygen-glucose deprivation/reoxygenation in PC12 cells and primary neurons to simulate cerebral ischemia/reperfusion injury. We found that prolongation of oxygen-glucose deprivation activated the ER stress pathway protein kinase-like endoplasmic reticulum kinase (PERK)/eukaryotic translation initiation factor 2 subunit alpha (eIF2α)-activating transcription factor 4 (ATF4)-C/EBP homologous protein (CHOP), increased neuronal apoptosis, and induced autophagy. Furthermore, inhibition of ER stress using inhibitors or by siRNA knockdown of the PERK gene significantly attenuated excessive autophagy and neuronal apoptosis, indicating an interaction between autophagy and ER stress and suggesting PERK as an essential target for regulating autophagy. Blocking autophagy with chloroquine exacerbated ER stress-induced apoptosis, indicating that normal levels of autophagy play a protective role in neuronal injury following cerebral ischemia/reperfusion injury. Findings from this study indicate that cerebral ischemia/ reperfusion injury can trigger neuronal ER stress and promote autophagy, and suggest that PERK is a possible target for inhibiting excessive autophagy in cerebral ischemia/reperfusion injury.","PeriodicalId":506566,"journal":{"name":"Neural Regeneration Research","volume":"513 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140480022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0