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Mannitol inhibits the proliferation of neural stem cell by a p38 mitogen-activated protein kinase-dependent signaling pathway

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Chinese Journal of Traumatology 2024年第1期27卷 42-52页

作者： Hai-Zhen Duan Xin Zhou Quan Hu Meng-Long Liu Shu-Hong Wang Ji Zhang Xu-Heng Jiang Tian-Xi Zhang An-Yong Yu Department of Emergency Affiliated Hospital of Zunyi Medical UniversityZunyi563000Guizhou provinceChina Dazhou Vocational College of Chinese Medicine Dazhou635000Sichuan provinceChina Dachuan District Traditional Chinese Medicine Hospital Dazhou635000Sichuan provinceChina

Purpose:Mannitol is one of the first-line drugs for reducing cerebral edema through increasing the extracellular osmotic pressure.However,long-term administration of mannitol in the treatment of cerebral edema triggers damage to neurons and astrocytes.Given that neural stem cell(NSC)is a subpopulation of main regenerative cells in the central nervous system after injury,the effect of mannitol on NSC is still elusive.The present study aims to elucidate the role of mannitol in NSC proliferation.Methods:C57 mice were derived from the animal house of Zunyi Medical University.A total of 15 pregnant mice were employed for the purpose of isolating NSCs in this investigation.Initially,mouse primary NSCs were isolated from the embryonic cortex of mice and subsequently identified through immunofluorescence staining.In order to investigate the impact of mannitol on NSC proliferation,both cell counting kit-8 assays and neurospheres formation assays were conducted.Thein vitro effects of mannitol were examined at various doses and time points.In order to elucidate the role of Aquaporin 4(aqp4)in the suppressive effect of mannitol on NSC proliferation,various assays including reverse transcription polymerase chain reaction,western blotting,and immunocytochemistry were conducted on control and mannitol-treated groups.Additionally,the phosphorylated p38(p-p38)was examined to explore the potential mechanism underlying the inhibitory effect of mannitol on NSC proliferation.Finally,to further confirm the involvement of the p38 mitogen-activated protein kinase-dependent(MAPK)signaling pathway in the observed inhibition of NSC proliferation by mannitol,SB203580 was employed.All data were analyzed using SPSS 20.0 software(SPSS,Inc.,Chicago,IL).The statistical analysis among multiple comparisons was performed using one-way analysis of variance(ANOVA),followed by Turkey’’s post hoc test in case of the data following a normal distribution using a Shapiro-Wilk normality test.Comparisons between 2 groups were determined using Student’s t-te

关键词： Mannitol Cerebral edema Neural stem cell Proliferation aqp4 p38 MAPK signaling pathway

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Anti-aquaporin-4 antibody(aqp4-IgG)and anti-myelin oligodendrocyte glycoprotein antibody(MOG-IgG)in the cerebrospinal fluid

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Neural Regeneration Research 2024年第5期19卷 949-950页

作者： Tetsuya Akaishi Tatsuro Misu Department of Neurology Tohoku UniversitySendaiJapan

In the last decade,a new neurological disease concept known as anti-myelin oligodendrocyte glycoprotein antibody(MOG-IgG)-associated disease(MOGAD)has emerged and is currently one of the most focused research areas in the field of neuroimmunology.MOG is a membrane protein mainly expressed on the surface of oligodendrocytes(Zhou et al.,2006).The exact pathogenic role of MOG-IgG in patients with MOGAD remains unclear;however,MOG-IgG has been suggested to cause tissue alterations and damage MOG-expressing cells(Zhou et al.,2006).The pathogenicity of MOG-IgG is further supported by the observation that only a few patients with acquired central nervous system(CNS)demyelinating syndromes exhibit both anti-aquaporin-4 antibody(aqp4-IgG)and MOG-IgG simultaneously,particularly with clear positivity levels of these antibodies as indicated by a cell-based assay result with a titer≥1:100(Sechi et al.,2021;Banwell et al.,2023).

关键词： aqp4 myelin

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Statistical evaluation of cluster formation of relapse in neuromyelitis optica spectrum disorder

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Neural Regeneration Research 2024年第9期19卷 1888-1889页

作者： Tetsuya Akaishi Ichiro Nakashima Department of Neurology Tohoku UniversitySendaiJapan Department of Neurology Tohoku Medical and Pharmaceutical UniversitySendaiJapan

Evaluating the cluster formation of clinical attacks in chronic relapsing diseases is an important statistical issue because the presence of attack clusters may influence therapeutic strategies for relapse prevention.We recently reported the occurrence of unevenly clustered attacks in patients with anti-aquaporin-4(aqp4)antibody-positive neuromyelitis optica spectrum disorder(NMOSD)(Akaishi et al.,2020a).

关键词： aqp4 relapse

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Anti-BCMA CAR T-cell therapy CT103A in relapsed or refractory aqp4-IgG seropositive neuromyelitis optica spectrum disorders:phase 1 trial interim results

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Signal Transduction and Targeted Therapy 2023年第2期8卷 683-691页

作者： Chuan Qin Dai-Shi Tian Luo-Qi Zhou Ke Shang Liang Huang Ming-Hao Dong Yun-Fan You Jun Xiao Ying Xiong Wen Wang Hao Pang Jing-Jing Guo Song-Bai Cai Di Wang Chun-Rui Li Min Zhang Bi-Tao Bu Wei Wang Department of Neurology Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology430030 WuhanChina Hubei Key Laboratory of Neural Injury and Functional Reconstruction Huazhong University of Science and Technology430030 WuhanChina Department of Hematology Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology430030 WuhanChina Department of Radiology Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology430030 WuhanChina Nanjing IASO Biotherapeutics Ltd NanjingChina

Chimeric antigen receptor(CAR)T-cell therapy that targets B-cell maturation antigen(BCMA)have great potentials in autoimmune diseases and could be novel therapeutics for relapsed/refractory neuromyelitis optica spectrum disorder(NMOSD).To evaluate the safety and efficacy of the CT103A,a self-developed BCMA-targeting CAR construct against BCMA,in patients with aqp4-IgG seropositive NMOSD,an ongoing,investigator-initiated,open-label,single-arm,phase 1 clinical trial is conducted at our center.In total,12 patients were administered with a CAR-BCMA infusion.Ten of the 12 patients dosed were women(83.3%),with a median age of 49.5 years(range,30-67).were The most common events of grade 3 or higher were hematologic toxic effects.Seven patients(58%)developed infections,but no grade 4 infections occurred.Cytokine release syndrome was reported in all patients with only events of grade 1 or 2 observed.During the follow-up of a median 5.5 months,11 patients had no relapse;all patients generally reported improvement in disabilities and quality-of-life outcomes;11 patients’aqp-4 antibodies in serum showed a downward trend by the cutoff date.CAR T-cell expansion was associated with responses,and persisted more than 6 months post-infusion in 17%of the patients.In summary,CAR T-cell therapy shows a manageable safety profile and therapeutic potentials for patients with relapsed/refractory aqp4-IgG seropositive NMOSD.Another expansion phase is currently underway to determine the safety and efficacy of CAR T-BCMA infusion in patients with other neuro-inflammatory diseases.

关键词： aqp4 BCMA infusion

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Peripheral origin exosomal micro RNAs aggravate glymphatic system dysfunction in diabetic cognitive impairment

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药学学报:英文版 2023年第7期13卷 2817-2825页

作者： Lin Zhang Dongna Li Pengrong Yi Jiangwei Shi Mengqing Guo Qingsheng Yin Dingbin Liu Pengwei Zhuang Yanjun Zhang State Key Laboratory of Component-based Chinese Medicine Tianjin University of Traditional Chinese MedicineTianjin 301617China Haihe Laboratory of Modern Chinese Medicine Tianjin 301617China First Teaching Hospital of Tianjin University of Traditional Chinese Medicine Tianjin 300193China National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion Tianjin 300193China State Key Laboratory of Medicinal Chemical Biology Research Center for Analytical Sciencesand Tianjin Key Laboratory of Molecular Recognition and BiosensingCollege of ChemistryNankai UniversityTianjin 300071China

Cognitive dysfunction is one of the common central nervous systems(CNS)complications of diabetes mellitus,which seriously affects the quality of life of patients and results in a huge economic burden.The glymphatic system dysfunction mediated by aquaporin-4(aqp4)loss or redistribution in perivascular astrocyte endfeet plays a crucial role in diabetes-induced cognitive impairment(DCI).However,the mechanism of aqp4 loss or redistribution in the diabetic states remains unclear.Accumulating evidence suggests that peripheral insulin resistance target tissues and CNS communication affect brain homeostasis and that exosomal miRNAs are key mediators.Glucose and lipid metabolism disorder is an important pathological feature of diabetes mellitus,and skeletal muscle,liver and adipose tissue are the key target insulin resistance organs.In this review,the changes in exosomal miRNAs induced by peripheral metabolism disorders in diabetes mellitus were systematically reviewed.We focused on exosomal miRNAs that could induce low aqp4 expression and redistribution in perivascular astrocyte endfeet,which could provide an interorgan communication pathway to illustrate the pathogenesis of DCI.Furthermore,the mechanisms of exosome secretion from peripheral insulin resistance target tissue and absorption to the CNS were summarized,which will be beneficial for proposing novel and feasible strategies to optimize DCI prevention and/or treatment in diabetic patients.

关键词： Diabetic cognitive impairment aqp4 Peripheral-central communication Exosomal miRNAs Central nervous system Glymphatic system Diabetes mellitus Astrocyte

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Astrocytic aquaporin 4 subcellular translocation as a therapeutic target for cytotoxic edema in ischemic stroke

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Neural Regeneration Research 2022年第12期17卷 2666-2668页

作者： Adjanie Patabendige Ruoli Chen Department of Biology Edge Hill UniversityOrmskirkUK Brain Barriers Group School of Biomedical Sciences and PharmacyThe University of NewcastleCallaghanNSWAustralia School of Pharmacy and Bioengineering Keele UniversityNewcastle Under LymeStaffordshireUK

Brain edema is a common feature of several brain diseases(e.g.,stroke,traumatic brain injury,hydrocephalus,brain cancer,and brain infections).Brain edema leads to increased intracranial pressure and worsens outcomes in ischemic stroke patients.Conventional treatments to control brain edema,thus reducing intracranial pressure include different osmotherapeutics,hyperventilation,tromethamine,hypothermia,and barbiturate coma.However,level 1 evidence of efficacy is lacking for these treatments,with some being harmful rather than beneficial(Bardutzky and Schwab,2007).It has been proposed aquaporin 4(aqp4)can be a novel drug target for treating brain edema(Vandebroek and Yasui,2020).

关键词： aqp4 aquaporin treatment

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黄芩苷通过抑制星形胶质细胞TRPV4和aqp4治疗脑缺血再灌注引起的大鼠脑水肿

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中国中药杂志 2022年第4期47卷 1031-1038页

作者：郑晓宇宋文婷张业昊曹慧刘建勋北京中医药大学北京100029 中国中医科学院西苑医院基础医学研究所北京市中药药理重点实验室北京100091

该文旨在研究黄芩苷对脑缺血再灌注损伤所引起的脑水肿大鼠的药效学作用及作用机制,并从抑制星形胶质细胞肿胀的角度探讨治疗脑缺血再灌注损伤和脑水肿的有关机制,对相关中药治疗脑缺血疾病具有借鉴意义。实验中采用大脑中动脉闭塞法(... 详细信息

该文旨在研究黄芩苷对脑缺血再灌注损伤所引起的脑水肿大鼠的药效学作用及作用机制,并从抑制星形胶质细胞肿胀的角度探讨治疗脑缺血再灌注损伤和脑水肿的有关机制,对相关中药治疗脑缺血疾病具有借鉴意义。实验中采用大脑中动脉闭塞法(线栓法)制作大鼠脑缺血模型,将大鼠随机分为正常组、模型组、黄芩苷高剂量(20 mg·kg^(-1))组和黄芩苷低剂量(10 mg·kg^(-1))组,分别测定大鼠脑缺血后6、24 h的神经行为学、脑指数、脑含水量、脑梗死面积,大脑切片后采用苏木素-伊红(hematoxylin-eosin,HE)染色观察黄芩苷对脑皮层组织病理形态的影响,ELISA法测定脑组织中总谷胱甘肽(L-glutathione,GSH)和谷氨酸(glutamic acid,Glu)的含量,免疫印迹法(Western blot)测定脑组织中胶质纤维酸性蛋白(glial fibrillary acidic protein,GFAP)、水通道蛋白4(aquaporin-4,aqp4)、瞬时受体电位香草素受体4型通道(transient receptor potential vanilloid receptor 4,TRPV4)的含量,免疫组织化学染色法观察GFAP的表达情况,在机制探讨过程中采用黄芩苷低剂量组为给药组。实验结果显示,模型组大鼠的神经行为学评分(脑缺血6、24 h)、脑含水量和脑梗死面积均显著增加,黄芩苷高、低剂量均可降低大鼠的神经行为学评分、脑含水量和脑梗死面积;模型组大鼠脑组织中GSH的含量显著降低,Glu的含量显著增加,黄芩苷低剂量组可明显增加GSH的含量并降低Glu的含量;免疫组织化学染色可见模型组GFAP表达明显增加,星形胶质细胞肿胀并增殖,黄芩苷低剂量组可显著改善此情况;免疫印迹法结果显示,模型组大鼠脑皮层中GFAP、TRPV4、aqp4的表达均明显增加,黄芩苷低剂量组可显著降低它们的表达。病理学可见模型组大鼠大脑皮层结构损伤严重,黄芩苷低剂量组可明显改善皮层区病理损伤。以上结果表明,黄芩苷可有效改善大鼠脑缺血再灌注损伤所致的脑水肿,可能与通过抑制星形胶质细胞肿胀并抑制TRPV4和aqp4的通道开放有关。

关键词：黄芩苷星形胶质细胞脑缺血 GFAP aqp4 TRPV4

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Astrocytic modulation of potassium under seizures

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Neural Regeneration Research 2020年第6期15卷 980-987页

作者： Fushun Wang Xiaoming Qi Jun Zhang Jason HHuang Department of Neurosurgery Baylor Scott&White HealthTempleTXUSA Institute of Brain and Psychological Science Sichuan Normal UniversityChengduSichuan ProvinceChina Department of Neurosurgery PLA General HospitalBeijingChina Department of Surgery Texas A&M University College of MedicineTempleTXUSA

The contribution of an impaired astrocytic K^+ regulation system to epileptic neuronal hyperexcitability has been increasingly recognized in the last decade.A defective K^+ regulation leads to an elevated extracellular K^+ concentration([K^+]o).When[K^+]o reaches peaks of 10-12 mM,it is strongly associated with seizure initiation during hypersynchronous neuronal activities.On the other hand,reactive astrocytes during a seizure attack restrict influx of K^+ across the membrane both passively and actively.In addition to decreased K^+ buffering,aberrant Ca^2+ signaling and declined glutamate transport have also been observed in astrogliosis in epileptic specimens,precipitating an increased neuronal discharge and induction of seizures.This review aims to provide an overview of experimental findings that implicated astrocytic modulation of extracellular K^+ in the mechanism of epileptogenesis.

关键词： aqp4 Ca^2+ signaling cell volume connexins epilepsy K^+ buffering mi RNA NKCC pannexin TBI

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Regulatory effect of miRNA 320a on expression of aquaporin 4 in brain tissue of epileptic rats

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Asian Pacific Journal of Tropical Medicine 2015年第10期8卷 791-796页

作者： Yu-Cheng Song Wen-Juan Li Liu-Zhi Li Department of Neurology Shandong Ankang Hospital Institute of Forensic Medicine and Laboratory Medicine Jining Medical University

Objective:To study the expression of miRNA 320 a in the brain tissue of epileptic rats and analyze its effect on the expression of aquaporin 4(aqp4).Methods:All rats were performed with the intraperitoneal injection of lithium chloride(3 mmol/kg) and then the intraperitoneal injection of pilocarpine(30 mg/kg) 24 h later(injected twice) to prepare the epileptic model of Wistar rats.Rats in the control group were injected with the equal volume of normal saline.According to the Racine scale,rats with over stage 3 of epilepsy were chosen and the brain tissue was separated quickly and then stored at-80 ℃.The immunohistochemistry was used to detect the expression of aquaporin in the brain tissue of epileptic model and the Real-time PCR was employed to determine the difference in the expression of miRNA 320 a and aqp4 in the brain tissue of rats between the epileptic model group and control one.Five 5-day neonatal Wistar rats were chosen to collect the cerebral cortex and their primary astrocytes were separated and cultured.They were transfected with miRNA mimic and imitated to the endogenous miRNA 320 a to up-regulate the expression of miRNA 320 a.Results:In the model group,the expression of aqp4 was significantly higher than the control group(Paqp4.In the primary astrocytes,the transfection of miRNA 320 a mimic could significantly reduce the expression of aqp4,while its inhibitor could up-regulate the expression of aqp4,which indicated that miRNA 320 a could reduce the expression of aqp4.Conclusions:In the primary astrocytes of rats,the miRNA 320 a could inhibit the expression of aqp4 and after adding the inhibitor of miRNA 320 a,the expression of aqp4 was up-regulated.

关键词： miRNA 320a Epilepsy Aquaporin aqp4

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Both IDO1 and TDO contribute to the malignancy of gliomas via the Kyn–AhR–aqp4 signaling pathway

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Signal Transduction and Targeted Therapy 2020年第1期5卷 2348-2360页

作者： Lisha Du Zikang Xing Bangbao Tao Tianqi Li Dan Yang Weirui Li Yuanting Zheng Chunxiang Kuang Qing Yang State Key Laboratory of Genetic Engineering School of Life SciencesFudan UniversitySonghu Road 2005Shanghai 200438China Department of Neurosurgery Xinhua HospitalShanghai Jiaotong UniversitySchool of MedicineKongjiang Road 1665Shanghai 200092China Department of Chemistry Tongji UniversitySiping Road 1239Shanghai 200092China Institute of Science and Technology for Brain-Inspired Intelligence Fudan UniversityHandan Road 220Shanghai 200433China

Indoleamine 2,3-dioxygenase 1(IDO1),indoleamine 2,3-dioxygenase 2(IDO2),and tryptophan 2,3-dioxygenase(TDO)initiate the first step of the kynurenine pathway(KP),leading to the transformation of L-tryptophan(Trp)into L-kynurenine(Kyn)and other downstream metabolites.Kyn is known as an endogenous ligand of the aryl hydrocarbon receptor(AhR).Activation of AhR through TDO-derived Kyn is a novel mechanism to support tumor growth in gliomas.However,the role of IDO1 and IDO2 in this mechanism is still unknown.Herein,by using clinical samples,we found that the expression and activity of IDO1 and/or TDO(IDO1/TDO)rather than IDO2 were positively correlated with the pathologic grades of gliomas.The expression of IDO1/TDO rather than IDO2 was positively correlated with the Ki67 index and overall survival.The expression of IDO1/TDO was positively correlated with the expression of aquaporin 4(aqp4),implying the potential involvement of IDO1/TDO in glioma cell motility.Mechanistically,we found that IDO1/TDO accounted for the release of Kyn,which activated AhR to promote cell motility via the Kyn–AhR–aqp4 signaling pathway in U87MG glioma cells.RY103,an IDO1/TDO dual inhibitor,could block the IDO1/TDO–Kyn–AhR–aqp4 signaling pathway and exert anti-glioma effects in GL261 orthotopic glioma mice.Together,our results showed that the IDO1/TDO–Kyn–AhR–aqp4 signaling pathway is a new mechanism underlying the malignancy of gliomas,and suggest that both IDO1 and TDO might be valuable therapeutic targets for gliomas.

关键词： IDO1 aqp4 glioma

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