Pub Date : 2024-07-10DOI: 10.4103/nrr.nrr-d-24-00471
E. Ambrosini, A. Lanciotti, M. S. Brignone
{"title":"Calcium-sensitive protein MLC1 as a possible modulator of the astrocyte functional state","authors":"E. Ambrosini, A. Lanciotti, M. S. Brignone","doi":"10.4103/nrr.nrr-d-24-00471","DOIUrl":"https://doi.org/10.4103/nrr.nrr-d-24-00471","url":null,"abstract":"","PeriodicalId":506566,"journal":{"name":"Neural Regeneration Research","volume":"35 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141660381","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}
Pub Date : 2024-07-10DOI: 10.4103/nrr.nrr-d-24-00284
R. Socodato, João B. Relvas
{"title":"Neuroinflammation revisited through the microglial lens","authors":"R. Socodato, João B. Relvas","doi":"10.4103/nrr.nrr-d-24-00284","DOIUrl":"https://doi.org/10.4103/nrr.nrr-d-24-00284","url":null,"abstract":"","PeriodicalId":506566,"journal":{"name":"Neural Regeneration Research","volume":"28 48","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141659610","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}
{"title":"New insights on the role of chondroitin sulfate proteoglycans in neural stem cell–mediated repair in spinal cord injury","authors":"Seyed Mojtaba Hosseini, Soheila Karimi-Abdolrezaee","doi":"10.4103/nrr.nrr-d-24-00378","DOIUrl":"https://doi.org/10.4103/nrr.nrr-d-24-00378","url":null,"abstract":"","PeriodicalId":506566,"journal":{"name":"Neural Regeneration Research","volume":"38 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141660467","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}
Pub Date : 2024-07-10DOI: 10.4103/nrr.nrr-d-24-00334
P. Cartas-Cejudo, Adriana Cortés, Mercedes Lachén-Montes, Elena Anaya-Cubero, Joaquín Fernández-Irigoyen, E. Santamaría
{"title":"Data-driven drug repositioning using olfactory omics profiles: challenges and perspectives in neurodegeneration","authors":"P. Cartas-Cejudo, Adriana Cortés, Mercedes Lachén-Montes, Elena Anaya-Cubero, Joaquín Fernández-Irigoyen, E. Santamaría","doi":"10.4103/nrr.nrr-d-24-00334","DOIUrl":"https://doi.org/10.4103/nrr.nrr-d-24-00334","url":null,"abstract":"","PeriodicalId":506566,"journal":{"name":"Neural Regeneration Research","volume":"8 8","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141660907","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}
Pub Date : 2024-07-10DOI: 10.4103/nrr.nrr-d-24-00424
Anup Bhusal, Won-Ha Lee, K. Suk
{"title":"PGLYRP1 protein as a novel mediator of cellular dialogue in neuroinflammation","authors":"Anup Bhusal, Won-Ha Lee, K. Suk","doi":"10.4103/nrr.nrr-d-24-00424","DOIUrl":"https://doi.org/10.4103/nrr.nrr-d-24-00424","url":null,"abstract":"","PeriodicalId":506566,"journal":{"name":"Neural Regeneration Research","volume":"7 17","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141661542","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}
Pub Date : 2024-07-10DOI: 10.4103/nrr.nrr-d-24-00351
Haoqi Sun, Shiqian Shen, Robert J. Thomas, M. Westover, Can Zhang
{"title":"Sleep as a window to understand and regulate Alzheimer’s disease: emerging roles of thalamic reticular nucleus","authors":"Haoqi Sun, Shiqian Shen, Robert J. Thomas, M. Westover, Can Zhang","doi":"10.4103/nrr.nrr-d-24-00351","DOIUrl":"https://doi.org/10.4103/nrr.nrr-d-24-00351","url":null,"abstract":"","PeriodicalId":506566,"journal":{"name":"Neural Regeneration Research","volume":"11 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141660142","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}
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.
{"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}
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.
{"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}
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.
多项研究表明，未折叠蛋白反应和内质网（ER）应激的激活在严重脑缺血/再灌注损伤中起着至关重要的作用。自噬发生在脑缺血后数小时内，但ER应激与自噬之间的关系仍不清楚。在这项研究中，我们在 PC12 细胞和原代神经元中建立了氧-葡萄糖剥夺/复氧实验模型，以模拟脑缺血/再灌注损伤。我们发现，延长氧-葡萄糖剥夺可激活ER应激通路蛋白激酶样内质网激酶（PERK）/真核翻译起始因子2亚基α（eIF2α）-激活转录因子4（ATF4）-C/EBP同源蛋白（CHOP），增加神经元凋亡并诱导自噬。此外，使用抑制剂或通过 siRNA 敲除 PERK 基因来抑制 ER 应激，可显著减轻过度自噬和神经元凋亡，这表明自噬和 ER 应激之间存在相互作用，并提示 PERK 是调节自噬的一个重要靶点。用氯喹阻断自噬会加剧ER应激诱导的细胞凋亡，这表明正常水平的自噬在脑缺血再灌注损伤后的神经元损伤中起保护作用。本研究的结果表明，脑缺血/再灌注损伤可引发神经元ER应激并促进自噬，并提示PERK可能是抑制脑缺血/再灌注损伤中过度自噬的靶点。
{"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}
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