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Transcription Factor CEBPD-Mediated WTAP Facilitates the Stemness, Growth, Migration and Glycolysis of Glioblastoma Stem Like Cells
IF 3.7 3区 医学
Neurochemical Research Pub Date : 2025-02-13 DOI: 10.1007/s11064-024-04321-7
Jiong Geng, Yun Shao, Yi Pu, Yiping Wu, Zhengxiang Yang
{"title":"Transcription Factor CEBPD-Mediated WTAP Facilitates the Stemness, Growth, Migration and Glycolysis of Glioblastoma Stem Like Cells","authors":"Jiong Geng,&nbsp;Yun Shao,&nbsp;Yi Pu,&nbsp;Yiping Wu,&nbsp;Zhengxiang Yang","doi":"10.1007/s11064-024-04321-7","DOIUrl":"10.1007/s11064-024-04321-7","url":null,"abstract":"<div><p>Glioblastoma stem like cells (GSCs) are a group of cells with strong tumorigenicity that exist in glioblastoma (GBM). Wilms tumor 1-associated protein (WTAP) is thought to promote the malignant process of GBM. However, whether WTAP regulates GSCs function to mediate GBM process is still unclear. The expression levels of WTAP and CCAAT/enhancer-binding protein delta (CEBPD) were examined by qRT-PCR and western blot. GSCs stemness, proliferation, apoptosis, and migration were assessed using sphere formation assay, CCK8 assay, EdU assay, colony formation assay, flow cytometry and transwell assay. Cell glycolysis was evaluated by testing glucose consumption and lactification. The regulation of CEBPD on WTAP was confirmed by ChIP assay and dual-luciferase reporter assay. In vivo experiments were performed to explore the effect of CEBPD/WTAP on the tumorigenicity of GSCs. WTAP and CEBPD had increased expression in GBM tissues and GSCs. Silencing of WTAP suppressed GSCs stemnness, proliferation, migration, glycolysis and promoted apoptosis. CEBPD could bind to WTAP promoter region to enhance its transcription. Besides, WTAP overexpression reversed the suppressive effect of CEBPD knockdown on GSCs stemnness, growth, migration and glycolysis in vitro, as well as the reducing effect on tumorigenicity of GSCs in vivo. CEBPD/WTAP axis played a vital role in regulating GSCs function, providing a potential therapy target for GBM.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143396747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
The Interplay Between Endoplasmic Reticulum Stress and Ferroptosis in Neurological Diseases
IF 3.7 3区 医学
Neurochemical Research Pub Date : 2025-02-10 DOI: 10.1007/s11064-025-04348-4
Tianyu Zhai, Bingbing Wang, Caizhen Shi, Can Zhang, Juan Shen, Xixuan Feng, Feng Gao, Yanling Yang, Kunpeng Jia, Lin Zhao
{"title":"The Interplay Between Endoplasmic Reticulum Stress and Ferroptosis in Neurological Diseases","authors":"Tianyu Zhai,&nbsp;Bingbing Wang,&nbsp;Caizhen Shi,&nbsp;Can Zhang,&nbsp;Juan Shen,&nbsp;Xixuan Feng,&nbsp;Feng Gao,&nbsp;Yanling Yang,&nbsp;Kunpeng Jia,&nbsp;Lin Zhao","doi":"10.1007/s11064-025-04348-4","DOIUrl":"10.1007/s11064-025-04348-4","url":null,"abstract":"<div><p>Many studies in the open literature have highlighted the critical roles of endoplasmic reticulum stress and ferroptosis in neurological diseases such as neurodegenerative diseases, brain injuries, and depression, indicating that they are involved in the onset and progression of these diseases. Therefore, it is essential to explore the regulatory mechanisms and potential interventions targeting endoplasmic reticulum stress and ferroptosis in neurological diseases. However, most existing research has primarily focused on the unidirectional mechanisms of endoplasmic reticulum stress and ferroptosis within the nervous system, with a lack of in-depth investigations into their interactions. In this paper, we first present an overview of the pathogenesis of endoplasmic reticulum stress and ferroptosis, along with their roles in neurological diseases. We then summarize the latest findings on the interaction mechanism between endoplasmic reticulum stress and ferroptosis from the perspectives of calcium iron homeostasis, reactive oxygen species, microenvironment, and related factors. Finally, we explore the potential molecular mechanisms and targeted interventions associated with endoplasmic reticulum stress and ferroptosis in neurological diseases.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143379858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Focusing on Formyl Peptide Receptors after Traumatic Spinal Cord Injury: from Immune Response to Neurogenesis
IF 3.7 3区 医学
Neurochemical Research Pub Date : 2025-02-07 DOI: 10.1007/s11064-025-04347-5
Ziheng Pu, Dan Luo, Beining Shuai, Yuzhao Xu, Mingyong Liu, Jianhua Zhao
{"title":"Focusing on Formyl Peptide Receptors after Traumatic Spinal Cord Injury: from Immune Response to Neurogenesis","authors":"Ziheng Pu,&nbsp;Dan Luo,&nbsp;Beining Shuai,&nbsp;Yuzhao Xu,&nbsp;Mingyong Liu,&nbsp;Jianhua Zhao","doi":"10.1007/s11064-025-04347-5","DOIUrl":"10.1007/s11064-025-04347-5","url":null,"abstract":"<div><p>The intricate pathophysiological cascades following spinal cord injury (SCI), encompassing cellular demise, axonal degeneration, and the formation of glial scars, pose formidable barriers to neural regeneration and restoration. Notably, neuroinflammation and glial scars emerge as pivotal barrier to post-SCI repair. Formyl peptide receptors (FPRs) emerge as critical regulators of immune responses, exerting significant influence over inflammatory modulation and nerve regeneration subsequent to SCI. Beyond their classical expression in myeloid cells, FPRs demonstrate a pronounced presence within the central nervous system (CNS) with roles in the progression of neurodegenerative disorders and neurological malignancies. Post-SCI, the equilibrium of the inflammatory microenvironment is recalibrated through the strategic modulation of FPRs, including facilitating a balance in microglial polarization, stimulating neural stem cells (NSCs) migration, and promoting neural axon elongation. These observations enlighten the potential of FPRs as innovative targets for neuronal regenerations bolstering SCI repair. This review endeavors to delineate the distribution and function of FPRs in the aftermath of SCI, with a special attention to their roles in inflammatory regulation, NSCs mobilization, and synaptic growth. By elucidating these mechanisms, we aspire to contribute novel insights and strategies for SCI therapy.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143362118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Naltrexone Alters Neurochemical and Behavioral Parameters in a Zebrafish Model of Repeated Alcohol Exposure
IF 3.7 3区 医学
Neurochemical Research Pub Date : 2025-02-07 DOI: 10.1007/s11064-025-04349-3
Henrique Teza Bernardo, Guilherme Lodetti, Ana Caroline Salvador de Farias, Karolyne de Pieri Pickler, Samira Leila Baldin, Eduardo Ronconi Dondossola, Eduardo Pacheco Rico
{"title":"Naltrexone Alters Neurochemical and Behavioral Parameters in a Zebrafish Model of Repeated Alcohol Exposure","authors":"Henrique Teza Bernardo,&nbsp;Guilherme Lodetti,&nbsp;Ana Caroline Salvador de Farias,&nbsp;Karolyne de Pieri Pickler,&nbsp;Samira Leila Baldin,&nbsp;Eduardo Ronconi Dondossola,&nbsp;Eduardo Pacheco Rico","doi":"10.1007/s11064-025-04349-3","DOIUrl":"10.1007/s11064-025-04349-3","url":null,"abstract":"<div><p>Between the neurotransmission systems modulated by alcohol, the opioid system has been receiving attention in studies that seek to understand its relationship to the effects of addictive substances and different neuropsychiatric disorders. The use of naltrexone stands out in determining the mechanisms of the opioid system, as it acts as an opioid antagonist and consequently generates neurochemical responses. This study aimed to evaluate the pharmacological modulation of opioids on behavioral and neurobiological aspects in adult zebrafish submitted to the protocol of repeated exposure to ethanol and treated with naltrexone. Opioid modulation using naltrexone has been shown to modulate anxiety-like behavior, presenting anxiolytic properties in isolation, in addition to reversing the anxiogenic effect of ethanol through the Novel tank and Light/dark test. Naltrexone increased serotonin and dopamine levels, while ethanol antagonized these effects. In contrast, the interaction between ethanol and naltrexone raised noradrenaline levels. Naltrexone altered glutamate levels, however, ethanol reversed it. Ethanol acted on glutamate transporters increasing their activities, while naltrexone treatment reduced activities. No significant results were found in the pro-oxidant parameters, however, ethanol reduced SOD activity while naltrexone reversed. The same occurred in CAT activity. Also, naltrexone up-regulated the expression of genes related to the dopaminergic, glutamatergic, and opioid systems. The genes used as markers of the inflammatory process and glial activity were modulated by ethanol and together with naltrexone, respectively. Taken together, our findings reinforce the importance of opioid signaling on biochemical and molecular bases related to neuropsychiatric behaviors and diseases, such as anxiety and substance dependence.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143362119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Improvements in Exercise for Alzheimer’s Disease: Highlighting FGF21-Induced Cerebrovascular Protection
IF 3.7 3区 医学
Neurochemical Research Pub Date : 2025-02-04 DOI: 10.1007/s11064-025-04350-w
Juan Wang, Xiangyuan Meng, Jialun Yang, Yingzhe Tang, Fanqi Zeng, Yiyang Wang, Zeyu Chen, Dandan Chen, Ruihan Zou, Wenfeng Liu
{"title":"Improvements in Exercise for Alzheimer’s Disease: Highlighting FGF21-Induced Cerebrovascular Protection","authors":"Juan Wang,&nbsp;Xiangyuan Meng,&nbsp;Jialun Yang,&nbsp;Yingzhe Tang,&nbsp;Fanqi Zeng,&nbsp;Yiyang Wang,&nbsp;Zeyu Chen,&nbsp;Dandan Chen,&nbsp;Ruihan Zou,&nbsp;Wenfeng Liu","doi":"10.1007/s11064-025-04350-w","DOIUrl":"10.1007/s11064-025-04350-w","url":null,"abstract":"<div><p>Alzheimer’s disease (AD) is the most common neurodegenerative disease. Currently, it has shown a trend of earlier onset, with most patients experiencing a progressive decline in cognitive function following the disease’s onset, which places a heavy burden on society and family. Since no drug cure for AD exists, exploring new ways for its treatment and prevention has become critical. Early vascular damage is an initial trigger for neuronal injury in AD, underscoring the importance of vascular health in the early stages of the disease. Patients with early AD experience abnormal blood-brain barrier transport of amyloid-β (Aβ) peptides, with excess Aβ being deposited in the cerebral vasculature. The toxic effects of Aβ lead to abnormalities in cerebrovascular structure and function. Fibroblast growth factor21 (FGF21) is an endocrine factor that positively regulates energy homeostasis and glucose-lipid metabolism. Notably, it is one of the effective targets for metabolic disease prevention and treatment. Recent studies have found that FGF21 has anti-aging and vasoprotective effects, with receptors for FGF21 present in the brain. Exercise stimulates the liver to produce large amounts of FGF21, which enters the blood-brain barrier with the blood to exert neurovascular protection. Therefore, we review the biological properties of FGF21, its role in the cerebrovascular structure and function in AD, and the mechanism of exercise-regulated FGF21 action on AD-related cerebrovascular changes, aiming to provide a new theoretical basis for using exercise to ameliorate degenerative neurological diseases.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143108032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Regulation by Trace Amine-Associated Receptor 1 (TAAR1) of Dopaminergic-GABAergic Interaction in the Striatum: Effects of the Enhancer Drug (-)BPAP
IF 3.7 3区 医学
Neurochemical Research Pub Date : 2025-02-04 DOI: 10.1007/s11064-025-04337-7
Laszlo G. Harsing Jr., Gábor Szénási, Balázs Fehér, Ildikó Miklya
{"title":"Regulation by Trace Amine-Associated Receptor 1 (TAAR1) of Dopaminergic-GABAergic Interaction in the Striatum: Effects of the Enhancer Drug (-)BPAP","authors":"Laszlo G. Harsing Jr.,&nbsp;Gábor Szénási,&nbsp;Balázs Fehér,&nbsp;Ildikó Miklya","doi":"10.1007/s11064-025-04337-7","DOIUrl":"10.1007/s11064-025-04337-7","url":null,"abstract":"<div><p>Although it is well documented that the striatal GABAergic projection neurons receive excitatory and inhibitory dopaminergic innervation via D1 and D2 receptors, the trace amine-associated receptor 1 (TAAR1)-mediated regulation of this neural connection is much less studied. The presence of TAAR1 was originally detected in brain aminergic neurons, with recent evidence indicating its presence in striatal GABAergic neurons as well. The objective of the present study was to demonstrate the role of TAAR1 and signaling in dopaminergic-GABAergic interaction in the neural circuitry of the striatum. Besides trace amines, which are considered natural ligands for TAAR1, series of different exogenous drugs were identified to act on this receptor. Using the dopaminergic activity enhancer compound (-)BPAP ((-)-1-(benzofuran-2-yl)-2-propylaminopentane HCl), a potential agonist for TAAR1, we have found that it increased the electrical stimulation-induced [<sup>3</sup>H]dopamine release in rat striatal slices. This effect of (-)BPAP occurred parallel with increases of [<sup>3</sup>H]GABA release in striatum when used in 10<sup>–13</sup>–10<sup>–11</sup> mol/L concentrations. The effects of (-)BPAP on the release of both neurotransmitters were bell-shaped. We speculated that the rising phase of the concentration-effect curves was evoked by an agonist effect of (-)BPAP on TAAR1 whereas the declining phase was a result of heterodimerization of TAAR1 with pre- and postsynaptic dopamine D2 receptors. The bell-shaped curves suggest that the (-)BPAP-induced heterodimerization of TAAR1 with dopamine D2 receptors may switch off TAAR1 signaling and switch on transduction coupled to D2 receptors. We also suggest that (-)BPAP increases synaptic strength in a hypothetical quadrilateral neuronal organization consisting of dopaminergic nerve ending, GABAergic neurons, trace amine-producing D cells, and supportive glial cell processes.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s11064-025-04337-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143108033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Yin Yang 1: Function, Mechanisms, and Glia
IF 3.7 3区 医学
Neurochemical Research Pub Date : 2025-02-04 DOI: 10.1007/s11064-025-04345-7
Ada G. Rodríguez-Campuzano, Francisco Castelán, Luisa C. Hernández-Kelly, Marie-Paule Felder-Schmittbuhl, Arturo Ortega
{"title":"Yin Yang 1: Function, Mechanisms, and Glia","authors":"Ada G. Rodríguez-Campuzano,&nbsp;Francisco Castelán,&nbsp;Luisa C. Hernández-Kelly,&nbsp;Marie-Paule Felder-Schmittbuhl,&nbsp;Arturo Ortega","doi":"10.1007/s11064-025-04345-7","DOIUrl":"10.1007/s11064-025-04345-7","url":null,"abstract":"<div><p>Yin Yang 1 is a ubiquitously expressed transcription factor that has been extensively studied given its particular dual transcriptional regulation. Yin Yang 1 is involved in various cellular processes like cell cycle progression, cell differentiation, DNA repair, cell survival and apoptosis among others. Its malfunction or alteration leads to disease and even to malignant transformation. This transcription factor is essential for the proper central nervous system development and function. The activity of Yin Yang 1 depends on its interacting partners, promoter environment and chromatin structure, however, its mechanistic activity is not completely understood. In this review, we briefly discuss the Yin Yang 1 structure, post-translational modifications, interactions, mechanistic functions and its participation in neurodevelopment. We also discuss its expression and critical involvement in the physiology and physiopathology of glial cells, summarizing the contribution of Yin Yang 1 on different aspects of cellular function.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s11064-025-04345-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143184657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
MTOR Promotes Astrocyte Activation and Participates in Neuropathic Pain through an Upregulation of RIP3
IF 3.7 3区 医学
Neurochemical Research Pub Date : 2025-02-01 DOI: 10.1007/s11064-025-04341-x
Bingru Dong, Danyang Li, Shasha Song, Na He, Shouwei Yue, Sen Yin
{"title":"MTOR Promotes Astrocyte Activation and Participates in Neuropathic Pain through an Upregulation of RIP3","authors":"Bingru Dong,&nbsp;Danyang Li,&nbsp;Shasha Song,&nbsp;Na He,&nbsp;Shouwei Yue,&nbsp;Sen Yin","doi":"10.1007/s11064-025-04341-x","DOIUrl":"10.1007/s11064-025-04341-x","url":null,"abstract":"<div><p>Neuropathic pain (NP), a chronic pain condition, is the result of abnormalities in both central and peripheral pain conduction pathways. Here, we investigated the underlying mechanisms associated with this effect. We found that following chronic constriction injury (CCI) surgery, there was an increase of mTOR in astrocytes and an activation of astrocytes within the spinal cord. Pharmacological inhibition of mTOR reversed CCI-induced hyperalgesia and neuroinflammation. Moreover, knockdown of astrocytic mTOR rescued the downregulation of spinal glutamate metabolism-related protein expression, underscoring the pivotal role of mTOR in modulating this pathway. Intriguingly, we observed that overexpression of mTOR, achieved via intrathecal administration of TSC2-shRNA, led to an upregulation of RIP3. Notably, pharmacological inhibition of RIP3, while ineffective in modulating mTOR activation, effectively eliminated the mTOR-induced astrocyte activation. Mechanistically, we found that mTOR controlled the expression of RIP3 in astrocytes through ITCH-mediated ubiquitination and an autophagy-dependent degradation. Taken together, our results reveal an unanticipated link between mTOR and RIP3 in promoting astrocyte activation, providing new avenues of investigation directed toward the management and treatment of NP.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s11064-025-04341-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Long Noncoding RNA ISA1 Protects Against Ischemic Brain Damage by Promoting the Transformation of Microglia Toward Anti-inflammatory Phenotype via the SOCS3/JAK2/STAT3 Pathway
IF 3.7 3区 医学
Neurochemical Research Pub Date : 2025-02-01 DOI: 10.1007/s11064-025-04343-9
Ermei Lu, Peng Zhou, Yuanyuan Li, Jiale Chen, Kexin Zhang, Kecheng Zhou
{"title":"Long Noncoding RNA ISA1 Protects Against Ischemic Brain Damage by Promoting the Transformation of Microglia Toward Anti-inflammatory Phenotype via the SOCS3/JAK2/STAT3 Pathway","authors":"Ermei Lu,&nbsp;Peng Zhou,&nbsp;Yuanyuan Li,&nbsp;Jiale Chen,&nbsp;Kexin Zhang,&nbsp;Kecheng Zhou","doi":"10.1007/s11064-025-04343-9","DOIUrl":"10.1007/s11064-025-04343-9","url":null,"abstract":"<div><p>The shift of microglia towards an anti-inflammatory phenotype has been shown to decrease neuroinflammation, improve neurological function, and is considered a potential therapeutic approach for stroke. Abnormal expression of multiple long noncoding RNA (LncRNA) has been discovered to be crucially related to the pathogenesis progress of ischemic brain injury. Here we concentrated on a novel LncRNA NR_037961.1, which we named ischemic stroke associated LncRNA1 (LncRNA ISA1). The expression of LncRNA ISA1 was notably decreased in brain tissue of middle cerebral artery occlusion (MCAO) mice. Overexpression of LncRNA ISA1 decreases cerebral infarction and brain edema, and improves cerebral blood flow and neurological outcome, promoting recovery of MCAO mice. Additionally, the neuroprotective effects that LncRNA ISA1 plays on MCAO mice are mediated by encouraging the transformation of microglia toward anti-inflammatory phenotype and alleviating neuroinflammation. LncRNA ISA1 facilitates the phenotypic transformation of microglia, closely linked to its promotion of SOCS3 expression and subsequent inhibition of the JAK2/STAT3 signaling pathway. Furthermore, downregulation of SOCS3 eliminated the effects of LncRNA ISA1 on transformation of microglia to anti-inflammatory phenotype. Our results indicate that LncRNA ISA1 promotes the anti-inflammatory polarization of microglia via regulation of the SOCS3/JAK2/STAT3 signaling pathway, and contributes to its neuroprotective effects in ischemic stroke.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Dental Pulp Stem Cells Attenuate Early Brain Injury After Subarachnoid Hemorrhage via miR-26a-5p/PTEN/AKT Pathway
IF 3.7 3区 医学
Neurochemical Research Pub Date : 2025-01-30 DOI: 10.1007/s11064-025-04340-y
Peibang He, Hui Zhang, Jianfeng Wang, Yujia Guo, Qi Tian, Chengli Liu, Pian Gong, Qingsong Ye, Youjian Peng, Mingchang Li
{"title":"Dental Pulp Stem Cells Attenuate Early Brain Injury After Subarachnoid Hemorrhage via miR-26a-5p/PTEN/AKT Pathway","authors":"Peibang He,&nbsp;Hui Zhang,&nbsp;Jianfeng Wang,&nbsp;Yujia Guo,&nbsp;Qi Tian,&nbsp;Chengli Liu,&nbsp;Pian Gong,&nbsp;Qingsong Ye,&nbsp;Youjian Peng,&nbsp;Mingchang Li","doi":"10.1007/s11064-025-04340-y","DOIUrl":"10.1007/s11064-025-04340-y","url":null,"abstract":"<div><p>Subarachnoid hemorrhage (SAH) is a type of hemorrhagic stroke with high morbidity, mortality and disability, and early brain injury (EBI) after SAH is crucial for prognosis. Recently, stem cell therapy has garnered significant attention in the treatment of neurological diseases. Compared to other stem cells, dental pulp stem cells (DPSCs) possess several advantages, including abundant sources, absence of ethical concerns, non-invasive procurement, non-tumorigenic history and neuroprotective potential. Therefore, we aim to investigate whether DPSCs can improve EBI after SAH, and explore the mechanisms. In our study, we utilized the endovascular perforation method to establish a SAH mouse model and investigated whether DPSCs administered via tail vein injection could improve EBI after SAH. Furthermore, we used hemin-stimulated HT22 cells to simulate neuronal cell injury induced by SAH and employed a co-culture approach to examine the effects of DPSCs on these cells. To gain insights into the potential mechanisms underlying the improvement of SAH-induced EBI by DPSCs, we conducted bioinformatics analysis. Finally, we further validated our findings through experiments. In vivo experiments, we found that DPSCs administration improved neurological dysfunction, reduced brain edema, and prevented neuronal apoptosis in SAH mice. Additionally, we observed a decrease in the expression level of miR-26a-5p in the cortical tissues of SAH mice, which was significantly increased following intravenous injection of DPSCs. Through bioinformatic analysis and luciferase reporter assay, we confirmed the target relationship between miR-26a-5p and PTEN. Moreover, we demonstrated that DPSCs exerted neuroprotective effects by modulating the miR-26a-5p/PTEN/AKT pathway. Our study demonstrates that DPSCs can improve EBI after SAH through the miR-26a-5p/PTEN/AKT pathway, laying a foundation for the application of DPSCs in SAH treatment. These findings provide a theoretical basis for further investigating the therapeutic mechanisms of DPSCs and developing novel treatment strategies in SAH.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
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