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The delivery of miR-21a-5p by extracellular vesicles induces microglial polarization via the STAT3 pathway following hypoxia-ischemia in neonatal mice

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Neural Regeneration Research 2022年第10期17卷 2238-2246页

作者： Dan-Qing Xin Yi-Jing Zhao Ting-Ting Li Hong-Fei Ke Cheng-Cheng Gai Xiao-Fan Guo Wen-Qiang Chen De-Xiang Liu Zhen Wang Department of Physiology School of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina Department of Neurology Loma Linda University HealthLoma LindaCAUSA Department of Cardiology Qilu HospitalCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina Department of Medical Psychology and Ethics School of Basic Medicine SciencesCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina

Extracellular vesicles(EVs)from mesenchymal stromal cells(MSCs)have previously been shown to protect against brain injury caused by hypoxia-ischemia(HI).The neuroprotective effects have been found to relate to the anti-inflammatory effects of EVs.However,the underlying mechanisms have not previously been determined.In this study,we induced oxygen-glucose deprivation in BV-2 cells(a microglia cell line),which mimics HI in vitro,and found that treatment with MSCs-EVs increased the cell viability.The treatment was also found to reduce the expression of pro-inflammatory cytokines,induce the polarization of microglia towards the M2 phenotype,and suppress the phosphorylation of selective signal transducer and activator of transcription 3(STAT3)in the microglia.These results were also obtained in vivo using neonatal mice with induced HI.We investigated the potential role of miR-21a-5p in mediating these effects,as it is the most highly expressed miRNA in MSCs-EVs and interacts with the STAT3 pathway.We found that treatment with MSCs-EVs increased the levels of miR-21a-5p in BV-2 cells,which had been lowered following oxygen-glucose deprivation.When the level of miR-21a-5p in the MSCs-EVs was reduced,the effects on microglial polarization and STAT3 phosphorylation were reduced,for both the in vitro and in vivo HI models.These results indicate that MSCs-EVs attenuate HI brain injury in neonatal mice by shuttling miR-21a-5p,which induces microglial M2 polarization by targeting STAT3.

关键词： extracellular vesicles hypoxia-ischemia mesenchymal stromal cells microglia miR-21a-5p neuroinflammation oxygen-glucose deprivation STAT3

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hypoxia-ischemia in the immature rodent brain impairs serotonergic neuronal function in certain dorsal raphé nuclei

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Neural Regeneration Research 2020年第3期15卷 457-463页

作者： Hanna E.Reinebrant Julie A.Wixey Kathryn M.Buller UQ Centre for Clinical Research Faculty of Medicine The University of Queensland

Neonatal hypoxia-ischemia(HI)results in losses of serotonergic neurons in specific dorsal raphe nuclei.However,not all serotonergic raphe neurons are lost and it is therefore important to assess the function of remaining neurons in order to understand their potential to contribute to neurological disorders in the HI-affected neonate.The main objective of this study was to determine how serotonergic neurons,remaining in the dorsal raphe nuclei after neonatal HI,respond to an external stimulus(restraint stress).On postnatal day 3(P3),male rat pups were randomly allocated to one of the following groups:(i)control+no restraint(n=5),(ii)control+restraint(n=6),(iii)P3 HI+no restraint(n=5)or(iv)P3 HI+restraint(n=7).In the two HI groups,rat pups underwent surgery to ligate the common carotid artery and were then exposed to 6%O2 for 30 minutes.Six weeks after P3 HI,on P45,rats were subjected to restraint stress for 30 minutes.Using dual immunolabeling for Fos protein,a marker for neuronal activity,and serotonin(5-hydroxytrypamine;5-HT),numbers of Fos-positive 5-HT neurons were determined in five dorsal raphe nuclei.We found that restraint stress alone increased numbers of Fos-positive 5-HT neurons in all five dorsal raphe nuclei compared to control animals.However,following P3 HI,the number of stress-induced Fos-positive 5-HT neurons was decreased significantly in the dorsal raphe ventrolateral,interfascicular and ventral nuclei compared with control animals exposed to restraint stress.In contrast,numbers of stress-induced Fos-positive 5-HT neurons in the dorsal raphe dorsal and caudal nuclei were not affected by P3 HI.These data indicate that not only are dorsal raphe serotonergic neurons lost after neonatal HI,but also remaining dorsal raphe serotonergic neurons have reduced differential functional viability in response to an external stimulus.Procedures were approved by the University of Queensland Animal Ethics Committee(UQCCR958/08/NHMRC)on February 27,2009.

关键词： dorsal raphe nuclei Fos hypoxia-ischemia neonate newborn brain injury preterm restraint stress serotonin

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Transfer of mitochondria from mesenchymal stem cells derived from induced pluripotent stem cells attenuates hypoxia-ischemia-induced mitochondrial dysfunction in PC12 cells

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Neural Regeneration Research 2020年第3期15卷 464-472页

作者： Yan Yang Gen Ye Yue-Lin Zhang Hai-Wei He Bao-Qi Yu Yi-Mei Hong Wei You Xin Li Department of Emergency Medicine Department of Emergency and Critical Care MedicineGuangdong Provincial People’s HospitalGuangdong Academy of Medical SciencesGuangzhouGuangdong ProvinceChina Department of Emergency the First Affiliated HospitalSun Yat-sen UniversityGuangzhouGuangdong ProvinceChina Shantou University Medical College ShantouGuangdong ProvinceChina Department of Physiology and Pathophysiology School of Basic Medical SciencesCapital Medical UniversityKey Laboratory of Remodelling-related Cardiovascular DiseasesMinistry of EducationBeijingChina

Mitochondrial dysfunction in neurons has been implicated in hypoxia-ischemia-induced brain injury.Although mesenchymal stem cell therapy has emerged as a novel treatment for this pathology,the mechanisms are not fully understood.To address this issue,we first co-cultured 1.5×10^5 PC12 cells with mesenchymal stem cells that were derived from induced pluripotent stem cells at a ratio of 1:1,and then intervened with cobalt chloride(CoCl2)for 24 hours.Reactive oxygen species in PC12 cells was measured by Mito-sox.Mitochondrial membrane potential(ΔΨm)in PC12 cells was determined by JC-1 staining.Apoptosis of PC12 cells was detected by terminal deoxynucleotidal transferase-mediated dUTP nick end-labeling staining.Mitochondrial morphology in PC12 cells was examined by transmission electron microscopy.Transfer of mitochondria from the mesenchymal stem cells derived from induced pluripotent stem cells to damaged PC12 cells was measured by flow cytometry.Mesenchymal stem cells were induced from pluripotent stem cells by lentivirus infection containing green fluorescent protein in mitochondria.Then they were co-cultured with PC12 cells in Transwell chambers and treated with CoCl2 for 24 hours to detect adenosine triphosphate level in PC12 cells.CoCl2-induced PC12 cell damage was dose-dependent.Co-culture with mesenchymal stem cells significantly reduced apoptosis and restoredΔΨm in the injured PC12 cells under CoCl2 challenge.Co-culture with mesenchymal stem cells ameliorated mitochondrial swelling,the disappearance of cristae,and chromatin margination in the injured PC12 cells.After direct co-culture,mitochondrial transfer from the mesenchymal stem cells stem cells to PC12 cells was detected via formed tunneling nanotubes between these two types of cells.The transfer efficiency was greatly enhanced in the presence of CoCl2.More importantly,inhibition of tunneling nanotubes partially abrogated the beneficial effects of mesenchymal stem cells on CoCl2-induced PC12 cell injury.Mesenchymal stem cells reduced CoCl2-induced PC12

关键词： apoptosis brain injury hypoxia-ischemia induced pluripotent stem cells mesenchymal stem cells mitochondrial membrane potential mitochondrial transfer PC12 cells tunneling nanotubes

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Developmental changes of glutamate acid decarboxylase 67 in mouse brain after hypoxia ischemia

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Neuroscience Bulletin 2006年第1期22卷 47-51页

作者： Fa-Lin XU Chang-Lian ZHU Xiao-Yang WANG Department of Pediatrics the Third Affiliated Hospital of Zhengzhou University Zhengzhou 450052 China

Objective To study the developmental changes of glutamic acid decarboxylase-67 （ GAD-67, a GABA synthetic enzyme） in normal and hypoxic ischemic （HI） brain. Methods C57/BL6 mice on postnatal day （P） 5, 9, 21 and 60, corresponding developmentally to premature, term, juvenile and adult human brain were investigated by using both Western blot and immunohistochemistry methods either in normal condition or after hypoxic ischemic insult. Results The immunoreactivity of GAD67 was up regulated with brain development and significant difference was seen between mature （P21, P60） and immature （P5, P9） brain. GAD67 immunoreactivity decreased in the ipsilateral hemisphere in all the ages after hypoxia ischemia （HI） insult, but, significant decrease was only seen in the immature brain. Double labeling of GAD67 and cell death marker, TUNEL, in the cortex at 8h post-HI in the P9 mice showed that （15.6±7.0）% TUNEL positive cells were GAD67 positive which was higher than that of P60 mice. Conclusion These data suggest that GABAergic neurons in immature brain were more vulnerable to HI insult than that of mature brain.

关键词： glutamic acid decarboxylase brain development hypoxia-ischemia

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The critical role of the endolysosomal system in cerebral ischemia

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Neural Regeneration Research 2023年第5期18卷 983-990页

作者： Hui-Yi Zhang Ye Tian Han-Yan Shi Ya Cai Ying Xu Department of Anesthesiology Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina Department of Orthopedics Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina

Cerebral ischemia is a serious disease that triggers sequential pathological mechanisms, leading to significant morbidity and mortality. Although most studies to date have typically focused on the lysosome, a single organelle, current evidence supports that the function of lysosomes cannot be separated from that of the endolysosomal system as a whole. The associated membrane fusion functions of this system play a crucial role in the biodegradation of cerebral ischemia-related products. Here, we review the regulation of and the changes that occur in the endolysosomal system after cerebral ischemia, focusing on the latest research progress on membrane fusion function. Numerous proteins, including N-ethylmaleimide-sensitive factor and lysosomal potassium channel transmembrane protein 175, regulate the function of this system. However, these proteins are abnormally expressed after cerebral ischemic injury, which disrupts the normal fusion function of membranes within the endolysosomal system and that between autophagosomes and lysosomes. This results in impaired “maturation” of the endolysosomal system and the collapse of energy metabolism balance and protein homeostasis maintained by the autophagy-lysosomal pathway. Autophagy is the final step in the endolysosomal pathway and contributes to maintaining the dynamic balance of the system. The process of autophagosome-lysosome fusion is a necessary part of autophagy and plays a crucial role in maintaining energy homeostasis and clearing aging proteins. We believe that, in cerebral ischemic injury, the endolysosomal system should be considered as a whole rather than focusing on the lysosome. Understanding how this dynamic system is regulated will provide new ideas for the treatment of cerebral ischemia.

关键词： autophagy biodegradation brain injury chaperone-mediated autophagy endolysosomal system fusion hypoxia-ischemia brain mitophagy N-ethylmaleimide-sensitive protein TMEM175

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Acupuncture on intrauterine growth restriction associated brain injury:case study including use of magnetic resonance imaging

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Journal of Traditional Chinese Medicine 2023年第3期43卷 602-605页

作者： XIN Zhixiong LI Jiyuan XU Yanni LING Jing JIANG Min YU Yutian Department of Pediatrics People's Hospital of Sanshui DistrictFoshan 528000China Department of MRI Beijing Shijitan HospitalCapital Medical UniversityBeijing 100038China Ninth School of Clinical Medicine Peking UniversityBeijing 100038China Foshan Minfound Medical Imaging Diagnostic Center Foshan 528000China Department of Gynecology Shenzhen Traditional Chinese Medicine HospitalShenzhen 518033China Acupuncture Department Beijing Shijitan HospitalCapital Medical UniversityBeijing 100038China

Brain injury due to intrauterine growth restriction(IUGR) is a thorny clinical problem that often leads to permanent neurological deficits such as cerebral palsy.Few practical therapies can treat an IUGR-associated brain injury.We employed acupuncture to treat a 6-month-old male patient with severe hypoxic-ischemic encephalopathy(HIE) due to IUGR,as confirmed by magnetic resonance imaging(MRI).Three courses of acupuncture treatment significantly improved some of the patient’s clinical characteristics,such as his insensitive responsiveness and motor deficits,with remarkably reversed HIE features on MRI at 1-year of age.This case suggests that acupuncture is a potential treatment option for an IUGRassociated brain injury and warrants further investigation.

关键词： acupuncture fetal growth retardation brain injuries hypoxia-ischemia brain magnetic resonance imaging neuronal plasticity

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Glia and hemichannels: key mediators of perinatal encephalopathy

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Neural Regeneration Research 2018年第2期13卷 181-189页

作者： Robert Galinsky Joanne O.Davidson Justin M.Dean Colin R.Green Laura Bennet Alistair J.Gunn Department of Physiology University of Auckland The Ritchie Centre Hudson Institute of Medical Research Department of Ophthalmology University of Auckland

Perinatal encephalopathy remains a major cause of disability, such as cerebral palsy. Therapeutic hypo- thermia is now well established to partially reduce risk of disability in late preterm/term infants. However, new and complementary therapeutic targets are needed to further improve outcomes. There is increasing evidence that glia play a key role in neural damage after hypoxia-ischemia and infection/inflammation. In this review, we discuss the role of astrocytic gap junction （connexin） hemichannels in the spread of neural injury after hypoxia-ischemia and/or infection/inflammation. Potential mechanisms of hemichannel medi- ated injury likely involve impaired intraceUular calcium handling, loss of blood-brain barrier integrity and release of adenosine triphosphate （ATP） resulting in over-activation of purinergic receptors. We propose the hypothesis that inflammation-induced opening of connexin hemichannels is a key regulating event that initiates a vicious cycle of excessive ATP release, which in turn propagates activation of purinergic receptors on microglia and astrocytes. This suggests that developing new neuroprotective strategies for preterm infants will benefit from a detailed understanding of glial and connexin hemichannel responses.

关键词： hypoxia-ischemia connexin hemichannels spreading injury connexin 43 astrocytes hypoxicischemic encephalopathy

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Brain-derived neurotrophic factor and its related enzymes and receptors play important roles after hypoxic-ischemic brain damage

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Neural Regeneration Research 2021年第8期16卷 1453-1459页

作者： Liu-Lin Xiong Jie Chen Ruo-Lan Du Jia Liu Yan-Jun Chen Mohammed Al Hawwas Xin-Fu Zhou Ting-Hua Wang Si-Jin Yang Xue Bai National Traditional Chinese Medicine Clinical Research Base and Western Medicine Translational Medicine Research Center Department of Cardiovascular DiseaseAffiliated Traditional Chinese Medicine HospitalSouthwest Medical UniversityLuzhouSichuan ProvinceChina Cinical and Health Sciences University of South AustraliaAdelaideAustralia Animal Zoology Department Institute of NeuroscienceKunming Medical UniversityKunmingYunnan ProvinceChina Institute of Neurological Disease Translational Neuroscience CenterWest China HospitalSichuan UniversityChengduSichuan ProvinceChina

Brain-derived neurotrophic factor(BDNF) regulates many neurological functions and plays a vital role during the recovery from central nervous system injuries. However, the changes in BDNF expression and associated factors following hypoxia-ischemia induced neonatal brain damage, and the significance of these changes are not fully understood. In the present study, a rat model of hypoxic-ischemic brain damage was established through the occlusion of the right common carotid artery, followed by 2 hours in a hypoxic-ischemic environment. Rats with hypoxic-ischemic brain damage presented deficits in both sensory and motor functions, and obvious pathological changes could be detected in brain tissues. The m RNA expression levels of BDNF and its processing enzymes and receptors(Furin, matrix metallopeptidase 9, tissuetype plasminogen activator, tyrosine Kinase receptor B, plasminogen activator inhibitor-1, and Sortilin) were upregulated in the ipsilateral hippocampus and cerebral cortex 6 hours after injury;however, the expression levels of these m RNAs were found to be downregulated in the contralateral hippocampus and cerebral cortex. These findings suggest that BDNF and its processing enzymes and receptors may play important roles in the pathogenesis and recovery from neonatal hypoxic-ischemic brain damage. This study was approved by the Animal Ethics Committee of the University of South Australia(approval No. U12-18) on July 30, 2018.

关键词： brain injury brain-derived neurotrophic factor enzyme hypoxia-ischemia receptors recovery repair

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Transplantation of placenta-derived mesenchymal stem cells reduces hypoxic-ischemic brain damage in rats by ameliorating the inflammatory response

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Cellular & Molecular Immunology 2017年第8期14卷 693-701页

作者： Hongfang Ding Hui Zhang Huifang Ding Dong Li Xinhao Yi Xiaoxu Ma Ruijuan Li Mei Huang Xiuli Ju Department of Pediatrics Shengli Oil field Central Hospital31 Jinan RoadDongyingShandongChina Department of Neurology Qingdao Municipal Hospitalthe Affiliated Hospital of Medical College of Qingdao University1 Jiaozhou RoadQingdaoShandongChina Department of Pediatrics Qilu HospitalShandong University107 West Wenhua RoadJinanShandongChina

Hypoxic-ischemic brain damage(HIBD)is a common cause of infant death.The purpose of our research was to explore the immunoregulatory mechanism of placenta-derived mesenchymal stem cells(PD-MSCs)in HIBD treatment.Seven-day-old rat pups were randomly divided into HIBD,PD-MSC,fibroblast,and control groups.Forty-eight hours after HIBD induction,cells at a density of 5×104 cells/10μl were injected into the cerebral tissue in the PD-MSC and fibroblast groups.The TNF-α,interleukin-17(IL-17),interferon-γ(IFN-γ),and IL-10 levels were detected through quantitative real-time polymerase chain reaction(RT-PCR)and enzyme-linked immunosorbent assay(ELISA).Regulatory T cell(Tregs)populations were detected through flow cytometry,and forkhead box P3(Foxp3)was measured through western blot analysis.Behavioral tests and gross and pathological examinations showed that PD-MSC treatment exerted significantly stronger neuroprotective effects than the other treatments.The expression levels of pro-inflammatory cytokines were substantially upregulated after HI injury.Compared with fibroblast treatment,PD-MSC treatment inhibited the production of pro-inflammatory cytokines and increased the production of IL-10 in the ischemic hemispheres and peripheral blood serum(all P<0.01).Flow cytometry results showed a notable increase in the number of Tregs within the spleen of the HIBD group.Moreover,the number of Tregs and the Foxp3 expression levels were higher in the PD-MSC treatment group than in the HIBD and fibroblast groups(all P<0.01).Our research suggests that the mechanism of PD-MSC treatment for HIBD partially involves inflammatory response suppression.

关键词： cytokine hypoxia-ischemia mesenchymal stem cell neonatal rat regulatory T cell

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Recombinant Human Erythropoietin Augments Neovascularization Responses in a Neonatal Rat Model of Premature Brain Damage by Phosphatidylinositol 3 Kinase/Akt Pathway

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Chinese Medical Journal 2017年第7期130卷 854-858页

作者： Da-Fan Yu Li-Hua Zhu Li Jiang Department of Clinical Medcine Medical School of Southeast University Jiangsu 210009 China 2Department of Pediatrics Zhongda Hospital Southeast University Nanjing Jiangsu 210009 China

Background：Recombinant human-erythropoietin （rh-EPO） has therapeutic efficacy for premature infants with brain damage during the active rehabilitation and anti-inflammation.In the present study,we found that the rh-EPO was related to the promotion ofneovascularization.Our aim was to investigate whether rh-EPO augments neovascularization in the neonatal rat model of premature brain damage through the phosphatidylinositol 3 kinase （PI3K）/protein kinase B （Akt） signaling pathway.Methods：Postnatal day 5 （PD5）,rats underwent permanent ligation of the right common carotid artery and were exposed to hypoxia for 2 h.All the rat pups were randomized into five groups as follows：（1） control group;（2） hypoxia-ischemic （HI） group;（3） HI ＋ LY294002 group;（4） HI ＋ rh-EPO group;and （5） HI ＋ rh-EPO ＋ LY294002 group.The phospho-Akt protein was tested 90 min after the whole operation,and CD34,vascular endothelial growth factor receptor 2 （VEGFR2）,and vascular endothelial growth factor （VEGF） were also tested 2 days after the whole operation.Results：In the hypoxic and ischemic zone of the premature rat brain,the rh-EPO induced CD34＋ cells to immigrate to the HI brain zone （P 〈 0.05） and also upregulated the VEGFR2 protein expression （P 〈 0.05） and VEGF mRNA level （P 〈 0.05） through the PI3K/Akt （P 〈 0.05） signaling pathway when compared with other groups.Conclusions：The rh-EPO treatment augments neovascularization responses in the neonatal rat model of premature brain damage through the PI3K/Akt signaling pathway.Besides,the endogenous EPO may exist in the HI zone of rat brain and also has neovascularization function through the PI3K/Akt signaling pathway.

关键词： Erythropoietin hypoxia-ischemia Neovascularization Premature Brain

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