首页 > 最新文献

Glia最新文献

英文 中文
Therapeutic Potential of Growth Hormone in Peripheral Nerve Injury: Enhancing Schwann Cell Proliferation and Migration Through IGF-1R-AKT and ERK Signaling Pathways 生长激素在周围神经损伤中的治疗潜力:通过IGF-1R-AKT和ERK信号通路促进雪旺细胞增殖和迁移。
IF 5.4 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-11-28 DOI: 10.1002/glia.24653
Jiaqian Chen, Tingcheng Zhang, Chaohu Wang, Peirong Niu, Liehao Huang, Rongrong Guo, Chengdong Wu, Huarong Zhang, Zhiyong Wu, Songtao Qi, Yi Liu

Peripheral nerve injury (PNI) represents a prevalent condition characterized by the demyelination of affected nerves. The challenge of remyelinating these nerves and achieving satisfactory functional recovery has long been a persistent issue. The specific contributions of growth hormone (GH) in the aftermath of PNI have remained ambiguous. Our investigations have demonstrated that GH not only enhances neurological function scores but also promotes remyelination within a three-week period. Further in vivo studies corroborated that GH facilitates nerve function improvement by mitigating neuronal apoptosis. In vitro, the ideal concentration of GH for exerting effects on Schwann cells (SCs) has been identified as 80 ng/mL. Subsequent research uncovered GH's profound impact on SCs proliferation, cell cycle progression, and migration. Through RNA sequencing and additional experiments, it was discovered that GH treatment elevates the phosphorylation levels of IGF-1R, AKT, and ERK. Moreover, the GH-induced proliferation and migration of SCs were significantly diminished by the inhibition of the IGF-1R pathway, achieved through pre-treatment with Linsitinib. The outcomes of this investigation suggest that GH can significantly enhance the proliferation and migration of SCs, presenting it as a viable option for PNI repair.

周围神经损伤(PNI)是一种以受影响神经脱髓鞘为特征的普遍疾病。长期以来,对这些神经的髓鞘再生和实现令人满意的功能恢复的挑战一直是一个持久的问题。生长激素(GH)在PNI后的具体贡献仍然不明确。我们的研究表明生长激素不仅能提高神经功能评分,还能在三周内促进髓鞘再生。进一步的体内研究证实生长激素通过减轻神经元凋亡促进神经功能改善。体外,生长激素对雪旺细胞(SCs)发挥作用的理想浓度已被确定为80 ng/mL。随后的研究揭示了生长激素对SCs增殖、细胞周期进展和迁移的深远影响。通过RNA测序和其他实验,发现生长激素治疗可提高IGF-1R、AKT和ERK的磷酸化水平。此外,通过Linsitinib预处理,通过抑制IGF-1R通路,gh诱导的SCs增殖和迁移显著减少。本研究结果表明,生长激素可以显著增强SCs的增殖和迁移,这表明它是修复PNI的可行选择。
{"title":"Therapeutic Potential of Growth Hormone in Peripheral Nerve Injury: Enhancing Schwann Cell Proliferation and Migration Through IGF-1R-AKT and ERK Signaling Pathways","authors":"Jiaqian Chen,&nbsp;Tingcheng Zhang,&nbsp;Chaohu Wang,&nbsp;Peirong Niu,&nbsp;Liehao Huang,&nbsp;Rongrong Guo,&nbsp;Chengdong Wu,&nbsp;Huarong Zhang,&nbsp;Zhiyong Wu,&nbsp;Songtao Qi,&nbsp;Yi Liu","doi":"10.1002/glia.24653","DOIUrl":"10.1002/glia.24653","url":null,"abstract":"<div>\u0000 \u0000 <p>Peripheral nerve injury (PNI) represents a prevalent condition characterized by the demyelination of affected nerves. The challenge of remyelinating these nerves and achieving satisfactory functional recovery has long been a persistent issue. The specific contributions of growth hormone (GH) in the aftermath of PNI have remained ambiguous. Our investigations have demonstrated that GH not only enhances neurological function scores but also promotes remyelination within a three-week period. Further in vivo studies corroborated that GH facilitates nerve function improvement by mitigating neuronal apoptosis. In vitro, the ideal concentration of GH for exerting effects on Schwann cells (SCs) has been identified as 80 ng/mL. Subsequent research uncovered GH's profound impact on SCs proliferation, cell cycle progression, and migration. Through RNA sequencing and additional experiments, it was discovered that GH treatment elevates the phosphorylation levels of IGF-1R, AKT, and ERK. Moreover, the GH-induced proliferation and migration of SCs were significantly diminished by the inhibition of the IGF-1R pathway, achieved through pre-treatment with Linsitinib. The outcomes of this investigation suggest that GH can significantly enhance the proliferation and migration of SCs, presenting it as a viable option for PNI repair.</p>\u0000 </div>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 4","pages":"805-821"},"PeriodicalIF":5.4,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Single Cell Deletion of the Transcription Factors Trps1 and Sox9 in Astrocytes Reveals Novel Functions in the Adult Cerebral Cortex 星形胶质细胞中转录因子Trps1和Sox9的单细胞缺失揭示了成人大脑皮层的新功能。
IF 5.4 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-11-28 DOI: 10.1002/glia.24645
Poornemaa Natarajan, Christina Koupourtidou, Thibault de Resseguier, Manja Thorwirth, Riccardo Bocchi, Judith Fischer-Sternjak, Sarah Gleiss, Diana Rodrigues, Michael H. Myoga, Jovica Ninkovic, Giacomo Masserdotti, Magdalena Götz

Astrocytes play key roles in brain function, but how these are orchestrated by transcription factors (TFs) in the adult brain and aligned with astrocyte heterogeneity is largely unknown. Here we examined the localization and function of the novel astrocyte TF Trps1 (Transcriptional Repressor GATA Binding 1) and the well-known astrocyte TF Sox9 by Cas9-mediated deletion using Mokola-pseudotyped lentiviral delivery into the adult cerebral cortex. Trps1 and Sox9 levels showed heterogeneity among adult cortical astrocytes, which prompted us to explore the effects of deleting either Sox9 or Trps1 alone or simultaneously at the single-cell (by patch-based single-cell transcriptomics) and tissue levels (by spatial transcriptomics). This revealed TF-specific functions in astrocytes, such as synapse maintenance with the strongest effects on synapse number achieved by Trps1 deletion and a common effect on immune response. In addition, spatial transcriptomics showed non-cell-autonomous effects on the surrounding cells, such as oligodendrocytes and other immune cells with TF-specific differences on the type of immune cells: Trps1 deletion affecting monocytes specifically, while Sox9 deletion acting mostly on microglia and deletion of both TF affecting mostly B cells. Taken together, this study reveals novel roles of Trps1 and Sox9 in adult astrocytes and their communication with other glial and immune cells.

星形胶质细胞在脑功能中发挥着关键作用,但这些作用是如何由成人大脑中的转录因子(tf)协调的,以及星形胶质细胞的异质性是如何一致的,这在很大程度上是未知的。在这里,我们通过mokola -伪慢病毒传递到成人大脑皮层,通过cas9介导的缺失,研究了新型星形胶质细胞TF Trps1(转录抑制因子GATA结合1)和著名的星形胶质细胞TF Sox9的定位和功能。Trps1和Sox9水平在成人皮质星形胶质细胞中表现出异质性,这促使我们探索单独或同时删除Sox9或Trps1在单细胞(通过基于斑块的单细胞转录组学)和组织水平(通过空间转录组学)上的影响。这揭示了tf在星形胶质细胞中的特异性功能,如突触维持,其中Trps1缺失对突触数量的影响最大,对免疫反应的影响也很普遍。此外,空间转录组学对周围细胞,如少突胶质细胞和其他在免疫细胞类型上具有TF特异性差异的免疫细胞显示非细胞自主作用:Trps1缺失特异性影响单核细胞,而Sox9缺失主要作用于小胶质细胞,TF的缺失主要影响B细胞。综上所述,本研究揭示了Trps1和Sox9在成人星形胶质细胞及其与其他胶质细胞和免疫细胞的通讯中的新作用。
{"title":"Single Cell Deletion of the Transcription Factors Trps1 and Sox9 in Astrocytes Reveals Novel Functions in the Adult Cerebral Cortex","authors":"Poornemaa Natarajan,&nbsp;Christina Koupourtidou,&nbsp;Thibault de Resseguier,&nbsp;Manja Thorwirth,&nbsp;Riccardo Bocchi,&nbsp;Judith Fischer-Sternjak,&nbsp;Sarah Gleiss,&nbsp;Diana Rodrigues,&nbsp;Michael H. Myoga,&nbsp;Jovica Ninkovic,&nbsp;Giacomo Masserdotti,&nbsp;Magdalena Götz","doi":"10.1002/glia.24645","DOIUrl":"10.1002/glia.24645","url":null,"abstract":"<p>Astrocytes play key roles in brain function, but how these are orchestrated by transcription factors (TFs) in the adult brain and aligned with astrocyte heterogeneity is largely unknown. Here we examined the localization and function of the novel astrocyte TF Trps1 (Transcriptional Repressor GATA Binding 1) and the well-known astrocyte TF Sox9 by Cas9-mediated deletion using Mokola-pseudotyped lentiviral delivery into the adult cerebral cortex. Trps1 and Sox9 levels showed heterogeneity among adult cortical astrocytes, which prompted us to explore the effects of deleting either Sox9 or Trps1 alone or simultaneously at the single-cell (by patch-based single-cell transcriptomics) and tissue levels (by spatial transcriptomics). This revealed TF-specific functions in astrocytes, such as synapse maintenance with the strongest effects on synapse number achieved by Trps1 deletion and a common effect on immune response. In addition, spatial transcriptomics showed non-cell-autonomous effects on the surrounding cells, such as oligodendrocytes and other immune cells with TF-specific differences on the type of immune cells: Trps1 deletion affecting monocytes specifically, while Sox9 deletion acting mostly on microglia and deletion of both TF affecting mostly B cells. Taken together, this study reveals novel roles of Trps1 and Sox9 in adult astrocytes and their communication with other glial and immune cells.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 4","pages":"737-758"},"PeriodicalIF":5.4,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24645","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Modulation of OPC Mitochondrial Function by Inhibiting USP30 Promotes Their Differentiation 通过抑制 USP30 调节 OPC 线粒体功能可促进其分化。
IF 5.4 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-11-27 DOI: 10.1002/glia.24648
Allison L. Soung, Roxanne V. Kyauk, Shristi Pandey, Yun-An A. Shen, Mike Reichelt, Han Lin, Zhiyu Jiang, Praveen Kirshnamoorthy, Oded Foreman, Benjamin E. Lauffer, Tracy J. Yuen

Multiple lines of evidence indicate that mitochondrial dysfunction occurs in demyelinating diseases, such as multiple sclerosis (MS). Failure of remyelination is thought to be caused in part by a block of oligodendrocyte progenitor cell (OPC) differentiation into oligodendrocytes, which generate myelin sheaths around axons. The process of OPC differentiation requires a substantial amount of energy and high demand for ATP which is supplied through the mitochondria. In this study, we highlight mitochondrial gene expression changes during OPC differentiation in two murine models of remyelination and in human postmortem MS brains. Given these transcriptional alterations, we then investigate whether genetic alteration of USP30, a mitochondrial deubiquitinase, enhances OPC differentiation and myelination. By genetic knockout of USP30, we observe increased OPC differentiation and myelination without affecting OPC proliferation and survival in in vitro and ex vivo assays. We also find that OPC differentiation is accelerated in vivo following focal demyelination in USP30 knockout mice. The promotion of OPC differentiation and myelination observed is associated with increased oxygen consumption rates in USP30 knockout OPCs. Together, these data indicate a role for mitochondrial function and USP30 in OPC differentiation and myelination.

多种证据表明,多发性硬化症(MS)等脱髓鞘疾病会导致线粒体功能障碍。髓鞘再形成失败的部分原因被认为是少突胶质细胞祖细胞(OPC)向少突胶质细胞分化受阻,而少突胶质细胞可在轴突周围生成髓鞘。OPC 分化过程需要大量能量,对 ATP 的需求很高,而 ATP 是通过线粒体提供的。在本研究中,我们重点研究了两种小鼠再髓鞘化模型和人类死后多发性硬化症大脑中 OPC 分化过程中线粒体基因表达的变化。鉴于这些转录改变,我们随后研究了线粒体去泛素化酶 USP30 的基因改变是否会增强 OPC 分化和髓鞘化。通过基因敲除 USP30,我们观察到 OPC 分化和髓鞘化增强,而不影响体外和体内试验中 OPC 的增殖和存活。我们还发现,USP30基因敲除小鼠在体内发生局灶性脱髓鞘后,OPC分化会加速。观察到的 OPC 分化和髓鞘化的促进与 USP30 基因敲除 OPC 的耗氧量增加有关。这些数据共同表明了线粒体功能和 USP30 在 OPC 分化和髓鞘化过程中的作用。
{"title":"Modulation of OPC Mitochondrial Function by Inhibiting USP30 Promotes Their Differentiation","authors":"Allison L. Soung,&nbsp;Roxanne V. Kyauk,&nbsp;Shristi Pandey,&nbsp;Yun-An A. Shen,&nbsp;Mike Reichelt,&nbsp;Han Lin,&nbsp;Zhiyu Jiang,&nbsp;Praveen Kirshnamoorthy,&nbsp;Oded Foreman,&nbsp;Benjamin E. Lauffer,&nbsp;Tracy J. Yuen","doi":"10.1002/glia.24648","DOIUrl":"10.1002/glia.24648","url":null,"abstract":"<p>Multiple lines of evidence indicate that mitochondrial dysfunction occurs in demyelinating diseases, such as multiple sclerosis (MS). Failure of remyelination is thought to be caused in part by a block of oligodendrocyte progenitor cell (OPC) differentiation into oligodendrocytes, which generate myelin sheaths around axons. The process of OPC differentiation requires a substantial amount of energy and high demand for ATP which is supplied through the mitochondria. In this study, we highlight mitochondrial gene expression changes during OPC differentiation in two murine models of remyelination and in human postmortem MS brains. Given these transcriptional alterations, we then investigate whether genetic alteration of USP30, a mitochondrial deubiquitinase, enhances OPC differentiation and myelination. By genetic knockout of USP30, we observe increased OPC differentiation and myelination without affecting OPC proliferation and survival in in vitro and ex vivo assays. We also find that OPC differentiation is accelerated in vivo following focal demyelination in USP30 knockout mice. The promotion of OPC differentiation and myelination observed is associated with increased oxygen consumption rates in USP30 knockout OPCs. Together, these data indicate a role for mitochondrial function and USP30 in OPC differentiation and myelination.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 4","pages":"773-787"},"PeriodicalIF":5.4,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24648","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142724364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Unboxing “Omics” in Glial Biology to Understand Neurological Disease 揭开神经胶质生物学的 "Omics "神秘面纱,了解神经系统疾病。
IF 5.4 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-11-25 DOI: 10.1002/glia.24651
Jonathan R. Weinstein, Suman Jayadev, Shane Liddelow, B. J. L. Eggen
{"title":"Unboxing “Omics” in Glial Biology to Understand Neurological Disease","authors":"Jonathan R. Weinstein,&nbsp;Suman Jayadev,&nbsp;Shane Liddelow,&nbsp;B. J. L. Eggen","doi":"10.1002/glia.24651","DOIUrl":"10.1002/glia.24651","url":null,"abstract":"","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 3","pages":"448-450"},"PeriodicalIF":5.4,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142714989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Astrocytic GAT-3 Regulates Synaptic Transmission and Memory Formation in the Dentate Gyrus 星形胶质细胞 GAT-3 调节齿状回的突触传递和记忆形成
IF 5.4 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-11-21 DOI: 10.1002/glia.24649
Weida Shen, Fujian Chen, Yejiao Tang, Wen Zhou, Yulu Zhao, Xinrui Li, Jingyin Dong, Feng Zhu, Shishuo Chen, Ling-Hui Zeng

GABAergic network activity plays a crucial role in a wide array of physiological processes and is implicated in various pathological conditions. While extensive research has been conducted on how GABAergic network activity modulates both excitatory and inhibitory synaptic transmission in the CA1 region, the mechanisms by which it influences synaptic transmission in the entorhinal cortex-dentate gyrus (EC-DG) circuits are still largely unexplored. Using a combination of whole-cell patch-clamp recordings, optogenetics, immunohistochemistry, and behavioral assays, we demonstrate that activation of GABA transporter 3 (GAT-3) in astrocytes triggers an increase in intracellular Ca2+ via the reverse Na+/Ca2+ exchanger. Intriguingly, inhibiting GAT-3 impedes the GABA-induced elevation of astrocytic Ca2+ levels, thereby curtailing the subsequent enhancement of synaptic transmission. Additionally, we show that endogenously released GABA from interneurons also modulates synaptic transmission through GAT-3 in the DG. Crucially, by selectively diminishing astrocytic calcium signals, we observed a concomitant decrease in the GABA-induced enhancement of synaptic transmission, underscoring the crucial role of astrocytes in this regulatory pathway. Moreover, we found that the activation of GAT-3 enhances excitatory transmission via presynaptic GluN2B-containing N-methyl-D-aspartate receptors (GluN2B-NMDARs) in the DG. Finally, our in vivo experiments demonstrate that inhibiting GAT-3 adversely affects the formation of contextual fear memory, highlighting its pivotal role in cognitive processing. These findings underscore the significance of astrocytic GAT-3 in cognitive functions and offer valuable insights into potential therapeutic targets for cognitive impairments, opening new avenues for the treatment of related disorders.

GABA 能网络活动在一系列生理过程中起着至关重要的作用,并与各种病理状况有关。虽然关于 GABA 能网络活动如何调节 CA1 区兴奋性和抑制性突触传递的研究已经非常广泛,但它影响内侧皮层-齿状回(EC-DG)回路突触传递的机制在很大程度上仍未得到探索。利用全细胞膜片钳记录、光遗传学、免疫组织化学和行为测定等方法,我们证明了激活星形胶质细胞中的 GABA 转运体 3(GAT-3)会通过反向 Na+/Ca2+ 交换器引发细胞内 Ca2+ 的增加。耐人寻味的是,抑制 GAT-3 会阻碍 GABA 诱导的星形胶质细胞 Ca2+ 水平的升高,从而抑制随后的突触传递增强。此外,我们还发现,神经元间内源性释放的 GABA 也会通过 GAT-3 调节 DG 中的突触传递。最重要的是,通过选择性地减少星形胶质细胞的钙信号,我们观察到 GABA 诱导的突触传递增强也随之减少,这强调了星形胶质细胞在这一调节途径中的关键作用。此外,我们还发现,GAT-3 的激活会增强突触前 GluN2B 含 N-甲基-D-天冬氨酸受体(GluN2B-NMDARs)在 DG 中的兴奋传递。最后,我们的体内实验证明,抑制 GAT-3 会对情境恐惧记忆的形成产生不利影响,从而突出了它在认知处理过程中的关键作用。这些发现强调了星形胶质细胞 GAT-3 在认知功能中的重要作用,并为认知障碍的潜在治疗靶点提供了宝贵的见解,为相关疾病的治疗开辟了新的途径。
{"title":"Astrocytic GAT-3 Regulates Synaptic Transmission and Memory Formation in the Dentate Gyrus","authors":"Weida Shen,&nbsp;Fujian Chen,&nbsp;Yejiao Tang,&nbsp;Wen Zhou,&nbsp;Yulu Zhao,&nbsp;Xinrui Li,&nbsp;Jingyin Dong,&nbsp;Feng Zhu,&nbsp;Shishuo Chen,&nbsp;Ling-Hui Zeng","doi":"10.1002/glia.24649","DOIUrl":"10.1002/glia.24649","url":null,"abstract":"<div>\u0000 \u0000 <p>GABAergic network activity plays a crucial role in a wide array of physiological processes and is implicated in various pathological conditions. While extensive research has been conducted on how GABAergic network activity modulates both excitatory and inhibitory synaptic transmission in the CA1 region, the mechanisms by which it influences synaptic transmission in the entorhinal cortex-dentate gyrus (EC-DG) circuits are still largely unexplored. Using a combination of whole-cell patch-clamp recordings, optogenetics, immunohistochemistry, and behavioral assays, we demonstrate that activation of GABA transporter 3 (GAT-3) in astrocytes triggers an increase in intracellular Ca<sup>2+</sup> via the reverse Na<sup>+</sup>/Ca<sup>2+</sup> exchanger. Intriguingly, inhibiting GAT-3 impedes the GABA-induced elevation of astrocytic Ca<sup>2+</sup> levels, thereby curtailing the subsequent enhancement of synaptic transmission. Additionally, we show that endogenously released GABA from interneurons also modulates synaptic transmission through GAT-3 in the DG. Crucially, by selectively diminishing astrocytic calcium signals, we observed a concomitant decrease in the GABA-induced enhancement of synaptic transmission, underscoring the crucial role of astrocytes in this regulatory pathway. Moreover, we found that the activation of GAT-3 enhances excitatory transmission via presynaptic GluN2B-containing <i>N</i>-methyl-D-aspartate receptors (GluN2B-NMDARs) in the DG. Finally, our in vivo experiments demonstrate that inhibiting GAT-3 adversely affects the formation of contextual fear memory, highlighting its pivotal role in cognitive processing. These findings underscore the significance of astrocytic GAT-3 in cognitive functions and offer valuable insights into potential therapeutic targets for cognitive impairments, opening new avenues for the treatment of related disorders.</p>\u0000 </div>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 4","pages":"788-804"},"PeriodicalIF":5.4,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142685526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Microglia and Astrocytes in Postnatal Neural Circuit Formation 出生后神经回路形成中的小胶质细胞和星形胶质细胞
IF 5.4 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-11-21 DOI: 10.1002/glia.24650
Abigayle S. Duffy, Ukpong B. Eyo

Over the past two decades, microglia and astrocytes have emerged as critical mediators of neural circuit formation. Particularly during the postnatal period, both glial subtypes play essential roles in orchestrating nervous system development through communication with neurons. These functions include regulating synapse elimination, modulating neuronal density and activity, mediating synaptogenesis, facilitating axon guidance and organization, and actively promoting neuronal survival. Despite the vital roles of both microglia and astrocytes in ensuring homeostatic brain development, the extent to which the postnatal functions of these cells are regulated by sex and the manner in which these glial cells communicate with one another to coordinate nervous system development remain less well understood. Here, we review the critical functions of both microglia and astrocytes independently and synergistically in mediating neural circuit formation, focusing our exploration on the postnatal period from birth to early adulthood.

过去二十年来,小胶质细胞和星形胶质细胞已成为神经回路形成的关键介质。特别是在出生后时期,这两种神经胶质亚型通过与神经元的交流,在协调神经系统发育方面发挥着至关重要的作用。这些功能包括调节突触消除、调节神经元密度和活性、介导突触生成、促进轴突导向和组织,以及积极促进神经元存活。尽管小胶质细胞和星形胶质细胞在确保大脑平衡发育方面发挥着重要作用,但人们对这些细胞的产后功能在多大程度上受性别调节以及这些胶质细胞相互沟通以协调神经系统发育的方式仍然知之甚少。在这里,我们回顾了小胶质细胞和星形胶质细胞在独立和协同调解神经回路形成方面的关键功能,重点探讨了从出生到成年早期的产后阶段。
{"title":"Microglia and Astrocytes in Postnatal Neural Circuit Formation","authors":"Abigayle S. Duffy,&nbsp;Ukpong B. Eyo","doi":"10.1002/glia.24650","DOIUrl":"10.1002/glia.24650","url":null,"abstract":"<p>Over the past two decades, microglia and astrocytes have emerged as critical mediators of neural circuit formation. Particularly during the postnatal period, both glial subtypes play essential roles in orchestrating nervous system development through communication with neurons. These functions include regulating synapse elimination, modulating neuronal density and activity, mediating synaptogenesis, facilitating axon guidance and organization, and actively promoting neuronal survival. Despite the vital roles of both microglia and astrocytes in ensuring homeostatic brain development, the extent to which the postnatal functions of these cells are regulated by sex and the manner in which these glial cells communicate with one another to coordinate nervous system development remain less well understood. Here, we review the critical functions of both microglia and astrocytes independently and synergistically in mediating neural circuit formation, focusing our exploration on the postnatal period from birth to early adulthood.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 2","pages":"232-250"},"PeriodicalIF":5.4,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11662987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
All the single cells: Single-cell transcriptomics/epigenomics experimental design and analysis considerations for glial biologists 所有单细胞神经胶质生物学家的单细胞转录组学/表观组学实验设计和分析注意事项。
IF 5.4 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-11-19 DOI: 10.1002/glia.24633
Katherine E. Prater, Kevin Z. Lin

Single-cell transcriptomics, epigenomics, and other ‘omics applied at single-cell resolution can significantly advance hypotheses and understanding of glial biology. Omics technologies are revealing a large and growing number of new glial cell subtypes, defined by their gene expression profile. These subtypes have significant implications for understanding glial cell function, cell–cell communications, and glia-specific changes between homeostasis and conditions such as neurological disease. For many, the training in how to analyze, interpret, and understand these large datasets has been through reading and understanding literature from other fields like biostatistics. Here, we provide a primer for glial biologists on experimental design and analysis of single-cell RNA-seq datasets. Our goal is to further the understanding of why decisions are made about datasets and to enhance biologists’ ability to interpret and critique their work and the work of others. We review the steps involved in single-cell analysis with a focus on decision points and particular notes for glia. The goal of this primer is to ensure that single-cell ‘omics experiments continue to advance glial biology in a rigorous and replicable way.

以单细胞分辨率应用单细胞转录组学、表观基因组学和其他'omics'技术,可以极大地推动对神经胶质生物学的假设和理解。全能组学技术揭示了大量且日益增多的新神经胶质细胞亚型,这些亚型由其基因表达谱定义。这些亚型对了解神经胶质细胞功能、细胞间通讯以及神经胶质细胞在平衡状态和神经疾病等情况之间的特异性变化具有重要意义。对于许多人来说,如何分析、解释和理解这些大型数据集的培训都是通过阅读和理解生物统计学等其他领域的文献来进行的。在此,我们将为神经胶质生物学家提供有关单细胞 RNA-seq 数据集的实验设计和分析的入门指南。我们的目标是进一步了解数据集决策的原因,提高生物学家解释和评论自己和他人工作的能力。我们回顾了单细胞分析所涉及的步骤,重点是决策点和神经胶质细胞的特别注意事项。本入门指南的目的是确保单细胞'omics'实验继续以严谨和可复制的方式推进神经胶质生物学的发展。
{"title":"All the single cells: Single-cell transcriptomics/epigenomics experimental design and analysis considerations for glial biologists","authors":"Katherine E. Prater,&nbsp;Kevin Z. Lin","doi":"10.1002/glia.24633","DOIUrl":"10.1002/glia.24633","url":null,"abstract":"<p>Single-cell transcriptomics, epigenomics, and other ‘omics applied at single-cell resolution can significantly advance hypotheses and understanding of glial biology. Omics technologies are revealing a large and growing number of new glial cell subtypes, defined by their gene expression profile. These subtypes have significant implications for understanding glial cell function, cell–cell communications, and glia-specific changes between homeostasis and conditions such as neurological disease. For many, the training in how to analyze, interpret, and understand these large datasets has been through reading and understanding literature from other fields like biostatistics. Here, we provide a primer for glial biologists on experimental design and analysis of single-cell RNA-seq datasets. Our goal is to further the understanding of why decisions are made about datasets and to enhance biologists’ ability to interpret and critique their work and the work of others. We review the steps involved in single-cell analysis with a focus on decision points and particular notes for glia. The goal of this primer is to ensure that single-cell ‘omics experiments continue to advance glial biology in a rigorous and replicable way.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 3","pages":"451-473"},"PeriodicalIF":5.4,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142666550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
R-Ras1 and R-Ras2 regulate mature oligodendrocyte subpopulations R-Ras1和R-Ras2调控成熟的少突胶质细胞亚群。
IF 5.4 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-11-19 DOI: 10.1002/glia.24643
Berta Alcover-Sanchez, Gonzalo Garcia-Martin, Víctor Paleo-García, Ana Quintas, Ana Dopazo, Agnès Gruart, José María Delgado-García, Pedro de la Villa, Francisco Wandosell, Marta P. Pereira, Beatriz Cubelos

In the mammalian central nervous system, axonal myelination, executed by mature oligodendrocytes (MOLs), enables rapid neural transmission. Conversely, myelin deficiencies are hallmark features of multiple sclerosis, optic neuromyelitis, and some leukodystrophies. Recent studies have highlighted that MOLs are heterogeneous; however, how MOL subpopulations are specified and balanced in physiological settings is poorly understood. Previous works have demonstrated an essential role of the small GTPases R-Ras1 and R-Ras2 in the survival and myelination of oligodendrocytes. In this study, we aimed to determine how R-Ras1 and R-Ras2 contribute to the heterogeneity of MOL subpopulations. Our results evidence that R-Ras1 and R-Ras2 affect specification into the distinct subpopulations MOL1, MOL2, and MOL5/6, which in turn vary in their dependence of these GTPases. In R-Ras1 and/or R-Ras2 mutant mice, we observed an increase in the MOL1 subpopulation and a decrease in the MOL2 and MOL5/6 subpopulations. We identified R-Ras1 and R-Ras2 as key elements in balancing the heterogeneity of MOLs. Our results contribute to the understanding of the molecular mechanisms underlying the heterogeneity of MOLs and the myelination processes, which is crucial for innovating regenerative therapies for nervous system disorders.

在哺乳动物的中枢神经系统中,成熟少突胶质细胞(MOLs)的轴突髓鞘化使神经传输迅速。相反,髓鞘缺乏是多发性硬化症、视神经脊髓炎和某些白质营养不良症的标志性特征。最近的研究突出表明,髓鞘具有异质性;然而,人们对髓鞘亚群在生理环境中如何特定和平衡还知之甚少。之前的研究表明,小 GTP 酶 R-Ras1 和 R-Ras2 在少突胶质细胞的存活和髓鞘化过程中发挥着重要作用。在本研究中,我们旨在确定 R-Ras1 和 R-Ras2 如何导致 MOL 亚群的异质性。我们的研究结果证明,R-Ras1和R-Ras2影响了MOL1、MOL2和MOL5/6等不同亚群的分化,而这些亚群对这些GTP酶的依赖性又各不相同。在 R-Ras1 和/或 R-Ras2 突变小鼠中,我们观察到 MOL1 亚群增加,而 MOL2 和 MOL5/6 亚群减少。我们发现 R-Ras1 和 R-Ras2 是平衡 MOL 异质性的关键因素。我们的研究结果有助于人们了解MOLs异质性和髓鞘化过程的分子机制,这对于创新神经系统疾病的再生疗法至关重要。
{"title":"R-Ras1 and R-Ras2 regulate mature oligodendrocyte subpopulations","authors":"Berta Alcover-Sanchez,&nbsp;Gonzalo Garcia-Martin,&nbsp;Víctor Paleo-García,&nbsp;Ana Quintas,&nbsp;Ana Dopazo,&nbsp;Agnès Gruart,&nbsp;José María Delgado-García,&nbsp;Pedro de la Villa,&nbsp;Francisco Wandosell,&nbsp;Marta P. Pereira,&nbsp;Beatriz Cubelos","doi":"10.1002/glia.24643","DOIUrl":"10.1002/glia.24643","url":null,"abstract":"<p>In the mammalian central nervous system, axonal myelination, executed by mature oligodendrocytes (MOLs), enables rapid neural transmission. Conversely, myelin deficiencies are hallmark features of multiple sclerosis, optic neuromyelitis, and some leukodystrophies. Recent studies have highlighted that MOLs are heterogeneous; however, how MOL subpopulations are specified and balanced in physiological settings is poorly understood. Previous works have demonstrated an essential role of the small GTPases R-Ras1 and R-Ras2 in the survival and myelination of oligodendrocytes. In this study, we aimed to determine how R-Ras1 and R-Ras2 contribute to the heterogeneity of MOL subpopulations. Our results evidence that R-Ras1 and R-Ras2 affect specification into the distinct subpopulations MOL1, MOL2, and MOL5/6, which in turn vary in their dependence of these GTPases. In R-Ras1 and/or R-Ras2 mutant mice, we observed an increase in the MOL1 subpopulation and a decrease in the MOL2 and MOL5/6 subpopulations. We identified R-Ras1 and R-Ras2 as key elements in balancing the heterogeneity of MOLs. Our results contribute to the understanding of the molecular mechanisms underlying the heterogeneity of MOLs and the myelination processes, which is crucial for innovating regenerative therapies for nervous system disorders.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 4","pages":"701-719"},"PeriodicalIF":5.4,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24643","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142666551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Astrocytic NHERF-1 Increases Seizure Susceptibility by Inhibiting Surface Expression of TREK-1 星形胶质细胞 NHERF-1 通过抑制 TREK-1 的表面表达增加癫痫易感性
IF 5.4 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-11-14 DOI: 10.1002/glia.24644
Yeonju Bae, Soomin Lee, Ajung Kim, Shinae Lee, Seong-Seop Kim, Sunyoung Park, Junyeol Noh, Kanghyun Ryoo, Gwan-Su Yi, Jae-Yong Park, Eun Mi Hwang

Mature hippocampal astrocytes exhibit a linear current-to-voltage (I-V) K+ membrane conductance called passive conductance. It is estimated to enable astrocytes to keep potassium homeostasis in the brain. We previously reported that the TWIK-1/TREK-1 heterodimeric channels are crucial for astrocytic passive conductance. However, the regulatory mechanism of these channels by other binding proteins remains elusive. Here, we identified Na+/H+ exchange regulator-1 (NHERF-1), a protein highly expressed in astrocytes, as a novel interaction partner for these channels. NHERF-1 endogenously bound to TWIK-1/TREK-1 in hippocampal cultured astrocytes. When NHERF-1 is overexpressed or silenced, surface expression and activity of TWIK-1/TREK-1 heterodimeric channels are inhibited or enhanced, respectively. Furthermore, we confirmed that reduced astrocytic passive conductance by NHERF-1 overexpressing in the hippocampus increases kainic acid (KA)-induced seizure sensitivity. Taken together, these results suggest that NHERF-1 is a key regulator of TWIK-1/TREK-1 heterodimeric channels in astrocytes and suppression of TREK-1 surface expression by NHERF-1 increases KA-induced seizure susceptibility via reduction of astrocytic passive conductance.

成熟的海马星形胶质细胞表现出一种线性电流-电压(I-V)K+膜电导,称为被动电导。据估计,它能使星形胶质细胞在大脑中保持钾平衡。我们曾报道 TWIK-1/TREK-1 异源二聚体通道对星形胶质细胞的被动传导至关重要。然而,其他结合蛋白对这些通道的调控机制仍不明确。在这里,我们发现了一种在星形胶质细胞中高表达的蛋白--Na+/H+交换调节因子-1(NHERF-1)--是这些通道的新型相互作用伙伴。在海马培养的星形胶质细胞中,NHERF-1与TWIK-1/TREK-1内源结合。当 NHERF-1 过量表达或沉默时,TWIK-1/TREK-1 异源二聚体通道的表面表达和活性分别受到抑制或增强。此外,我们还证实,在海马中过表达 NHERF-1 会降低星形胶质细胞的被动传导性,从而增加凯尼酸(KA)诱导的癫痫发作敏感性。综上所述,这些结果表明,NHERF-1是星形胶质细胞中TWIK-1/TREK-1异源二聚体通道的关键调控因子,NHERF-1抑制TREK-1表面表达会通过降低星形胶质细胞的被动传导增加KA诱导癫痫发作的敏感性。
{"title":"Astrocytic NHERF-1 Increases Seizure Susceptibility by Inhibiting Surface Expression of TREK-1","authors":"Yeonju Bae,&nbsp;Soomin Lee,&nbsp;Ajung Kim,&nbsp;Shinae Lee,&nbsp;Seong-Seop Kim,&nbsp;Sunyoung Park,&nbsp;Junyeol Noh,&nbsp;Kanghyun Ryoo,&nbsp;Gwan-Su Yi,&nbsp;Jae-Yong Park,&nbsp;Eun Mi Hwang","doi":"10.1002/glia.24644","DOIUrl":"10.1002/glia.24644","url":null,"abstract":"<p>Mature hippocampal astrocytes exhibit a linear current-to-voltage (I-V) K<sup>+</sup> membrane conductance called passive conductance. It is estimated to enable astrocytes to keep potassium homeostasis in the brain. We previously reported that the TWIK-1/TREK-1 heterodimeric channels are crucial for astrocytic passive conductance. However, the regulatory mechanism of these channels by other binding proteins remains elusive. Here, we identified Na+/H+ exchange regulator-1 (NHERF-1), a protein highly expressed in astrocytes, as a novel interaction partner for these channels. NHERF-1 endogenously bound to TWIK-1/TREK-1 in hippocampal cultured astrocytes. When NHERF-1 is overexpressed or silenced, surface expression and activity of TWIK-1/TREK-1 heterodimeric channels are inhibited or enhanced, respectively. Furthermore, we confirmed that reduced astrocytic passive conductance by NHERF-1 overexpressing in the hippocampus increases kainic acid (KA)-induced seizure sensitivity. Taken together, these results suggest that NHERF-1 is a key regulator of TWIK-1/TREK-1 heterodimeric channels in astrocytes and suppression of TREK-1 surface expression by NHERF-1 increases KA-induced seizure susceptibility via reduction of astrocytic passive conductance.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 4","pages":"720-736"},"PeriodicalIF":5.4,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24644","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Aquaporin-4 activation facilitates glymphatic system function and hematoma clearance post-intracerebral hemorrhage 激活Aquaporin-4有助于脑出血后的肾上腺系统功能和血肿清除。
IF 5.4 2区 医学 Q1 NEUROSCIENCES Pub Date : 2024-11-12 DOI: 10.1002/glia.24639
Wenchao Chen, Chuntian Liang, Shasha Peng, Shuangjin Bao, Fang Xue, Xia Lian, Yinghong Liu, Gaiqing Wang

Efficient clearance of hematomas is crucial for improving clinical outcomes in patients with intracerebral hemorrhage (ICH). The glymphatic system, facilitated by aquaporin-4 (AQP4), plays a crucial role in cerebrospinal fluid (CSF) entry and metabolic waste clearance. This study examined the role of the glymphatic system in ICH pathology, with a focus on AQP4. Collagenase-induced ICH models were established, with AQP4 expression regulated through mifepristone as an agonist, TGN-020 as an inhibitor, and Aqp4 gene knockout. Fluorescence tracing and multimodal magnetic resonance imaging (MRI) were employed to observe glymphatic system functionality, hematoma, and edema volumes. Neurological deficit scoring was performed using the modified Garcia Scale. AQP4 expression was quantified using RT-qPCR and Western blotting, and cellular localization was explored using immunofluorescence. The brain tissue sections were examined for neuronal morphology, degenerative changes, and iron deposition. Three days post-ICH, the AQP4 agonist group showed increased AQP4 protein expression and perivascular polarization, decreased hemoglobin levels, and reduced iron deposition. Conversely, the inhibition group exhibited contrasting trends. AQP4 activation improved glymphatic system function, leading to a wider distribution, improved neurological function, and reduced hematoma. Pharmacological inhibition and genetic knockout of AQP4 have opposing effects. The glymphatic system, facilitated by AQP4, plays a crucial role in hematoma clearance following cerebral hemorrhage. Upregulation of AQP4 improves glymphatic system function, facilitates hematoma clearance, and promotes brain tissue recovery.

有效清除血肿对改善脑内出血(ICH)患者的临床疗效至关重要。由水汽蛋白-4(AQP4)促进的甘油系统在脑脊液(CSF)进入和代谢废物清除中发挥着至关重要的作用。本研究以 AQP4 为重点,探讨了甘液系统在 ICH 病理学中的作用。研究人员建立了胶原酶诱导的 ICH 模型,通过米非司酮作为激动剂、TGN-020 作为抑制剂以及 Aqp4 基因敲除来调节 AQP4 的表达。采用荧光追踪和多模态磁共振成像(MRI)观察甘回流系统功能、血肿和水肿体积。采用改良加西亚量表对神经功能缺损进行评分。使用 RT-qPCR 和 Western 印迹法量化 AQP4 的表达,并使用免疫荧光法检测细胞定位。对脑组织切片进行神经元形态、退行性变化和铁沉积检查。脑梗死三天后,AQP4 激动剂组显示 AQP4 蛋白表达和血管周围极化增加,血红蛋白水平降低,铁沉积减少。相反,抑制组则呈现出截然不同的趋势。激活 AQP4 可改善甘液系统功能,使其分布更广,改善神经功能,减少血肿。药物抑制和基因敲除 AQP4 的效果截然相反。在 AQP4 的促进下,甘液系统在脑出血后的血肿清除中发挥着至关重要的作用。上调 AQP4 可改善甘液系统功能,促进血肿清除,促进脑组织恢复。
{"title":"Aquaporin-4 activation facilitates glymphatic system function and hematoma clearance post-intracerebral hemorrhage","authors":"Wenchao Chen,&nbsp;Chuntian Liang,&nbsp;Shasha Peng,&nbsp;Shuangjin Bao,&nbsp;Fang Xue,&nbsp;Xia Lian,&nbsp;Yinghong Liu,&nbsp;Gaiqing Wang","doi":"10.1002/glia.24639","DOIUrl":"10.1002/glia.24639","url":null,"abstract":"<p>Efficient clearance of hematomas is crucial for improving clinical outcomes in patients with intracerebral hemorrhage (ICH). The glymphatic system, facilitated by aquaporin-4 (AQP4), plays a crucial role in cerebrospinal fluid (CSF) entry and metabolic waste clearance. This study examined the role of the glymphatic system in ICH pathology, with a focus on AQP4. Collagenase-induced ICH models were established, with AQP4 expression regulated through mifepristone as an agonist, TGN-020 as an inhibitor, and <i>Aqp4</i> gene knockout. Fluorescence tracing and multimodal magnetic resonance imaging (MRI) were employed to observe glymphatic system functionality, hematoma, and edema volumes. Neurological deficit scoring was performed using the modified Garcia Scale. AQP4 expression was quantified using RT-qPCR and Western blotting, and cellular localization was explored using immunofluorescence. The brain tissue sections were examined for neuronal morphology, degenerative changes, and iron deposition. Three days post-ICH, the AQP4 agonist group showed increased AQP4 protein expression and perivascular polarization, decreased hemoglobin levels, and reduced iron deposition. Conversely, the inhibition group exhibited contrasting trends. AQP4 activation improved glymphatic system function, leading to a wider distribution, improved neurological function, and reduced hematoma. Pharmacological inhibition and genetic knockout of AQP4 have opposing effects. The glymphatic system, facilitated by AQP4, plays a crucial role in hematoma clearance following cerebral hemorrhage. Upregulation of AQP4 improves glymphatic system function, facilitates hematoma clearance, and promotes brain tissue recovery.</p>","PeriodicalId":174,"journal":{"name":"Glia","volume":"73 2","pages":"368-380"},"PeriodicalIF":5.4,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11662979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142613212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Glia
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1