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Exosomes from Bone marrow mesenchymal stem cells are a potential treatment for ischemic stroke

Neural Regeneration Research 2023年第10期18卷 2246-2251页

作者： Chang Liu Tian-Hui Yang Hong-Dan Li Gong-Zhe Li Jia Liang Peng Wang Liaoning Provincial Key Laboratory of Neurodegenerative Diseases and Department of Neurobiology Jinzhou Medical UniversityJinzhouLiaoning ProvinceChina Institute of Life Science Jinzhou Medical UniversityJinzhouLiaoning ProvinceChina College of Pharmacy Jinzhou Medical UniversityJinzhouLiaoning ProvinceChina

Exosomes derived from human Bone marrow mesenchymal stem cells(MSC-Exo)are characterized by easy expansion and storage,low risk of tumor formation,low immunogenicity,and anti-inflammatory effects.The therapeutic effects of MSC-Exo on ischemic stroke have been widely explored.However,the underlying mechanism remains unclear.In this study,we established a mouse model of ischemic brain injury induced by occlusion of the middle cerebral artery using the thread bolt method and injected MSC-Exo into the tail vein.We found that administration of MSC-Exo reduced the volume of cerebral infarction in the ischemic brain injury mouse model,increased the levels of interleukin-33(IL-33)and suppression of tumorigenicity 2 receptor(ST2)in the penumbra of cerebral infarction,and improved neurological function.In vitro results showed that astrocyte-conditioned medium of cells deprived of both oxygen and glucose,to simulate ischemia conditions,combined with MSC-Exo increased the survival rate of primary cortical neurons.However,after transfection by IL-33 siRNA or ST2 siRNA,the survival rate of primary cortical neurons was markedly decreased.These results indicated that MSC-Exo inhibited neuronal death induced by oxygen and glucose deprivation through the IL-33/ST2 signaling pathway in astrocytes.These findings suggest that MSC-Exo may reduce ischemia-induced brain injury through regulating the IL-33/ST2 signaling pathway.Therefore,MSC-Exo may be a potential therapeutic method for ischemic stroke.

关键词： astrocytes Bone marrow mesenchymal stem cells brain injury exosome IL-33 inflammation ischemic stroke neurological function neuron ST2

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Exosomes derived from Bone marrow mesenchymal stem cells inhibit neuroinflammation after traumatic brain injury

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Neural Regeneration Research 2022年第12期17卷 2717-2724页

作者： Liang Wen Ya-Dong Wang Dong-Feng Shen Pei-Dong Zheng Meng-Di Tu Wen-Dong You Yuan-Run Zhu Hao Wang Jun-Feng Feng Xiao-Feng Yang The First Affiliated Hospital School of MedicineZhejiang UniversityHangzhouZhejiang ProvinceChina Department of Intensive Care Unit The First Hospital of JiaxingJiaxingZhejiang ProvinceChina Department of Neurosurgery Renji HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghaiChina

Exosomes derived from Bone marrow mesenchymal stem cells can inhibit neuroinflammation through regulating microglial phenotypes and promoting nerve injury repair.However,the underlying molecular mechanism remains unclear.In this study,we investigated the mechanism by which exosomes derived from Bone marrow mesenchymal stem cells inhibit neuroinflammation.Our in vitro co-culture experiments showed that Bone marrow mesenchymal stem cells and their exosomes promoted the polarization of activated BV2 microglia to their anti-inflammatory phenotype,inhibited the expression of proinflammatory cytokines,and increased the expression of anti-inflammatory cytokines.Our in vivo experiments showed that tail vein injection of exosomes reduced cell apoptosis in cortical tissue of mouse models of traumatic brain injury,inhibited neuroinflammation,and promoted the transformation of microglia to the anti-inflammatory phenotype.We screened some microRNAs related to neuroinflammation using microRNA sequencing and found that microRNA-181b seemed to be actively involved in the process.Finally,we regulated the expression of miR181b in the brain tissue of mouse models of traumatic brain injury using lentiviral transfection.We found that miR181b overexpression effectively reduced apoptosis and neuroinflamatory response after traumatic brain injury and promoted the transformation of microglia to the anti-inflammatory phenotype.The interleukin 10/STAT3 pathway was activated during this process.These findings suggest that the inhibitory effects of exosomes derived from Bone marrow mesenchymal stem cells on neuroinflamation after traumatic brain injury may be realized by the action of miR181b on the interleukin 10/STAT3 pathway.

关键词： apoptosis Bone marrow mesenchymal stem cells BV2 microglia exosome interleukin 10 lentiviral transfection microRNA-181b neuroinflammation phenotype signal transducer and activator of transcription 3 traumatic brain injury

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Exosomal miR-23b from Bone marrow mesenchymal stem cells alleviates oxidative stress and pyroptosis after intracerebral hemorrhage

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Neural Regeneration Research 2023年第3期18卷 560-567页

作者： Liu-Ting Hu Bing-Yang Wang Yu-Hua Fan Zhi-Yi He Wen-Xu Zheng Department of Neurology The First Affiliated HospitalSun Yat-Sen UniversityGuangzhouGuangdong ProvinceChina Department of Neurology The First Affiliated Hospital of China Medical UniversityShenyangLiaoning ProvinceChina Geriatric Department of Dalian Friendship Hospital DalianLiaoning ProvinceChina

Our previous studies showed that miR-23b was downregulated in patients with intracerebral hemorrhage(ICH). This indicates that miR-23b may be closely related to the patho-physiological mechanism of ICH, but this hypothesis lacks direct evidence. In this study, we established rat models of ICH by injecting collagenase Ⅶ into the right basal ganglia and treating them with an injection of bone marrow mesenchymal stem cell(BMSC)-derived exosomal miR-23b via the tail vein. We found that edema in the rat brain was markedly reduced and rat behaviors were improved after BMSC exosomal miR-23b injection compared with those in the ICH groups. Additionally, exosomal miR-23b was transported to the microglia/macrophages, thereby reducing oxidative stress and pyroptosis after ICH. We also used hemin to mimic ICH conditions in vitro. We found that phosphatase and tensin homolog deleted on chromosome 10(PTEN) was the downstream target gene of miR-23b, and exosomal miR-23b exhibited antioxidant effects by regulating the PTEN/Nrf2 pathway. Moreover, miR-23b reduced PTEN binding to NOD-like receptor family pyrin domain containing 3(NLRP3) and NLRP3 inflammasome activation, thereby decreasing the NLRP3-dependent pyroptosis level. These findings suggest that BMSC-derived exosomal miR-23b exhibits antioxidant effects through inhibiting PTEN and alleviating NLRP3 inflammasome-mediated pyroptosis, thereby promoting neurologic function recovery in rats with ICH.

关键词： Bone marrow mesenchymal stem cells exosomal miRNAs intracerebral hemorrhage miR-23b neuroinflammation NLRP3 inflammasome Nrf2 oxidative stress PTEN pyroptosis

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Effects of interleukin-10 treated macrophages on Bone marrow mesenchymal stem cells via signal transducer and activator of transcription 3 pathway

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World Journal of stem cells 2024年第5期16卷 560-574页

作者： Meng-Hao Lyu Ce Bian Yi-Ping Dou Kang Gao Jun-Ji Xu Pan Ma Department of Periodontics School of StomatologyCapital Medical UniversityBeijing 100050China Department of Orthodontics School of StomatologyCapital Medical UniversityBeijing 100050China Department of Dental Implantology School of StomatologyCapital Medical UniversityBeijing 100050China Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction School of StomatologyCapital Medical UniversityBeijing 100050China Beijing Laboratory of Oral Health Capital Medical UniversityBeijing 100050China

BACKGROUND Alveolar bone defects caused by inflammation are an urgent issue in oral implant surgery that must be solved.Regulating the various phenotypes of macrophages to enhance the inflammatory environment can significantly affect the progression of diseases and tissue engineering repair process.AIM To assess the influence of interleukin-10(IL-10)on the osteogenic differentiation of Bone marrow mesenchymal stem cells(BMSCs)following their interaction with macrophages in an inflammatory environment.METHODS IL-10 modulates the differentiation of peritoneal macrophages in Wistar rats in an inflammatory environment.In this study,we investigated its impact on the proliferation,migration,and osteogenesis of BMSCs.The expression levels of signal transducer and activator of transcription 3(STAT3)and its activated form,phos-phorylated-STAT3,were examined in IL-10-stimulated macrophages.Subsequently,a specific STAT3 signaling inhibitor was used to impede STAT3 signal activation to further investigate the role of STAT3 signaling.RESULTS IL-10-stimulated macrophages underwent polarization to the M2 type through substitution,and these M2 macrophages actively facilitated the osteogenic differentiation of BMSCs.Mechanistically,STAT3 signaling plays a crucial role in the process by which IL-10 influences macrophages.Specifically,IL-10 stimulated the activation of the STAT3 signaling pathway and reduced the macrophage inflammatory response,as evidenced by its diminished impact on the osteogenic differentiation of BMSCs.CONCLUSION Stimulating macrophages with IL-10 proved effective in improving the inflammatory environment and promoting the osteogenic differentiation of BMSCs.The IL-10/STAT3 signaling pathway has emerged as a key regulator in the macrophage-mediated control of BMSCs’osteogenic differentiation.

关键词： Macrophages Interleukin-10 Bone marrow mesenchymal stem cells Signal transducer and activator of transcription 3 Inflammatory response

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bone marrow-derived mesenchymal stem cells modulate autophagy in RAW264.7 macrophages via the phosphoinositide 3-kinase/protein kinase B/heme oxygenase-1 signaling pathway under oxygen-glucose deprivation/restoration conditions

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Chinese Medical Journal 2021年第6期134卷 699-707页

作者： Ning-Fang Wang Chun-Xue Bai Department of Pulmonary Medicine Zhongshan HospitalFudan UniversityShanghai 200032China

Background: Autophagy of alveolar macrophages is a crucial process in ischemia/reperfusion injury-induced acute lung injury (ALI). bone marrow-derived mesenchymal stem cells (BM-MSCs) are multipotent cells with the potential for repairing injured sites and regulating autophagy. This study was to investigate the influence of BM-MSCs on autophagy of macrophages in the oxygen-glucose deprivation/restoration (OGD/R) microenvironment and to explore the potential mechanism.Methods: We established a co-culture system of macrophages (RAW264.7) with BM-MSCs under OGD/R conditionsin vitro. RAW264.7 cells were transfected with recombinant adenovirus (Ad-mCherry-GFP-LC3B) and autophagic status of RAW264.7 cells was observed under a fluorescence microscope. Autophagy-related proteins light chain 3 (LC3)-I, LC3-II, and p62 in RAW264.7 cells were detected by Western blotting. We used microarray expression analysis to identify the differently expressed genes between OGD/R treated macrophages and macrophages co-culture with BM-MSCs. We investigated the gene heme oxygenase-1 (HO-1), which is downstream of the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway.Results: The ratio of LC3-II/LC3-I of OGD/R treated RAW264.7 cells was increased (1.27 ± 0.20vs. 0.44 ± 0.08,t = 6.67,P cells (0.68 ± 0.14vs. 1.27 ± 0.20,t = 4.12,P < 0.05), up-regulated p62 expression (1.10 ± 0.20vs. 0.77 ± 0.04,t = 2.80,P < 0.05), and up-regulated PI3K (0.54 ± 0.05vs. 0.40 ± 0.06,t = 3.11,P < 0.05) and p-Akt/Akt ratios (0.52 ± 0.05vs. 0.39 ± 0.02,t = 9.13,P < 0.05). A whole-genome microarray assay screened the differentially expressed geneHO-1, which is downstream of the PI3K/Akt signaling pathway, and the alteration ofHO-1 mRNA and pr

关键词： Bone marrow mesenchymal stem cells Oxygen-glucose deprivation/restoration Phosphoinositide 3-kinase/protein kinase B signaling pathway Macrophages Autophagy Whole-genome microarray assay

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Transplantation of BMP-7 gene-transfected Bone marrow mesenchymal stem cells for the treatment of spinal cord injury in rats

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BIOCELL 2022年第9期46卷 2065-2072页

作者： XUYI WANG WEN ZHANG LEI GAO KUANXIN LI Department of Orthopedics The First Affiliated Hospital of Bengbu Medical CollegeBengbu233000China Department of Orthopedics The Second Affiliated Hospital of Medical College of Shihezi UniversityUrumqi832000China Department of Spinal Surgery The Second Affiliated Hospital of Medical College of Shihezi UniversityUrumqi832000China

Background:Spinal cord injury(SCI)is a serious traumatic disease of the central nervous system,and there is currently no effective treatment for SCI because of its complicated pathophysiology.Bone marrow mesenchymal stem cells(BMSCs)have multidirectional differentiation abilities.Our study aims to explore the effects of bone morphogenetic protein 7(BMP-7)-modified BMSCs transplantation on the repair of SCI in rats.Methods:In this study,a rat spinal cord injury model was established with the modified Allen method.Then,BMSCs transfected with the BMP7 gene were transplanted to treat the spinal cord injury in rats.Forty Sprague-Dawley rats were randomly divided into the sham operation group(sham group),spinal cord injury group(model group),BMSC treatment group(BMSC group)and LV-BMP7-BMSC treatment group(LV-BMP7-BMSC group).The Basso,Beattie,and Bresnahan(BBB)score was used to evaluate the recovery of hindlimb function in the rats.The levels of neurofilament protein NF-200(NF-200)and glial fibrillary acidic protein(GFAP)were detected by immunofluorescence,RT-PCR and Western blotting.Results:At 14 d,21 d,and 28 d after treatment,the BBB score of the rats in the LV-BMP7-BMSC group was higher than that of the rats in the model group and BMSC group.The results showed that NF-200 was expressed at the local spinal cord injury site.Compared with that of the sham group,the NF-200 expression level of the BMSC group and LV-BMP7-BMSC group was increased(P<0.05).The results showed that the mRNA expression levels of NF-200 in the spinal cord tissue of the BMSC group and LV-BMP7-BMSC group were increased compared with those of the sham group(P<0.05).The western blotting results further confirmed the PCR results.Conclusion:BMP-7 gene-modified BMSC transplantation can promote the repair of spinal cord functions after SCI in rats.

关键词： bone morphogenetic protein 7 Bone marrow mesenchymal stem cells Spinal cord injury

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A novel mutation in ROR2 led to the loss of function of ROR2 and inhibited the osteogenic differentiation capability of Bone marrow mesenchymal stem cells(BMSCs)

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BIOCELL 2023年第7期47卷 1561-1569页

作者： WENQI CHEN XIAOYANG CHU YANG ZENG YOUSHENG YAN YIPENG WANG DONGLAN SUN DONGLIANG ZHANG JING ZHANG KAI YANG Prenatal Diagnosis Center Shijiazhuang Obstetrics and Gynecology HospitalKey Laboratory of Maternal and Fetal Medicine of Hebei ProvinceShijiazhuang050011China Department of Stomatology Fifth Medical Center of Chinese PLA General HospitalBeijing100039China Institute of Hematology Fifth Medical Center of Chinese PLA General HospitalBeijing100039China Prenatal Diagnosis Center Beijing Obstetrics and Gynecology HospitalBeijing Maternal and Child Health Care HospitalCapital Medical UniversityBeijing100026China Department of Orthodontics Beijing Stomatological HospitalCapital Medical University School of StomatologyCapital Medical UniversityBeijing100050China

Receptor tyrosine kinase-like orphan receptor 2(ROR2)has a vital role in osteogenesis.However,the mechanism underlying the regulation of ROR2 in osteogenic differentiation is still poorly comprehended.A previous study by our research group showed that a novel compound heterozygous ROR2 variation accounted for the autosomal recessive Robinow syndrome(ARRS).This study attempted to explore the impact of the ROR2:c.904C>T variant specifically on the osteogenic differentiation of BMSCs.Methods:Coimmunoprecipitation(CoIP)-western blotting was carried out to identify the interaction between ROR2 and Wnt5a.Double-immunofluorescence staining was used for determining the expressions and co-localization of ROR2 and Wnt5a in Bone marrow mesenchymal stem cells(BMSCs).Western blot(WB)analysis and quantitative reverse transcription polymerase chain reaction(RT-qPCR)were conducted to identify the expression levels of ROR2 in the BMSCs transfected with LV-shROR2 or LV-ROR2-c.904C>T.The alkaline phosphatase(ALP)activity was detected,and Alizarin Red S staining was done for evaluating the osteogenic differentiation of BMSCs.RT-qPCR was employed to identify the expression of the sphingomyelin synthase 1(SMS1)mRNA in the BMSCs transfected with LV-shROR2 or LV-ROR2-c.904C>T and the mRNA expression levels of Runt-related transcription factor 2(RUNX2),osteocalcin(OCN),and osteopontin(OPN).WB was performed to confirm the protein expressions of extracellular regulated protein kinases1(ERK),P-ERK,Smad family member1/5/8(Smad1/5/8),P-Smad1/5/8,P-P38,P38,RUNX2,OCN,and OPN in the BMSCs transfected with LV-shROR2/LV-ROR2-c.904C>T and sphingomyelin(SM).Results:The ROR2:c.904C>T mutant altered the subcellular localization of the ROR2 protein,which caused an impaired interaction between ROR2 and Wnt5a.The depletion of ROR2 restricted the osteogenic differentiation capability of BMSCs and downregulated the expression of SMS1.SM treatment could reverse the inhibition of osteoblastic differentiation in ROR2-depleted BMSCs.Conclusion:The findings of

关键词： Bone marrow mesenchymal stem cells ROR2 Wnt5a Osteogenic differentiation Sphingomyelin

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Transplantation of Bone marrow mesenchymal stem cells improves cognitive deficits and alleviates neuropathology in animal models of Alzheimer’s disease: a meta-analytic review on potential mechanisms

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Translational Neurodegeneration 2020年第2期9卷 214-233页

作者： Chuan Qin Yalan Lu Kewei Wang Lin Bai Guiying Shi Yiying Huang Yongning Li Institute of Laboratory Animal Sciences Chinese Academy of Medical Sciences&Comparative Medical CenterPeking Union Medical CollegeBeijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases5 Panjiayuan Nanli StBeijing100021China Department of International Medical Service&Department of Neurosurgery Peking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeShuaifuyuan 1Dong Cheng DistrictBeijing100730China

Background Alzheimer’s disease is a neurodegenerative disorder.Therapeutically,a transplantation of Bone marrow mesenchymal stem cells(BMMSCs)can play a beneficial role in animal models of Alzheimer’s disease.However,the relevant mechanism remains to be fully elucidated.Main body Subsequent to the transplantation of BMMSCs,memory loss and cognitive impairment were significantly improved in animal models with Alzheimer’s disease(AD).Potential mechanisms involved neurogenesis,apoptosis,angiogenesis,inflammation,immunomodulation,etc.The above mechanisms might play different roles at certain stages.It was revealed that the transplantation of BMMSCs could alter some gene levels.Moreover,the differential expression of representative genes was responsible for neuropathological phenotypes in Alzheimer’s disease,which could be used to construct gene-specific patterns.Conclusions Multiple signal pathways involve therapeutic mechanisms by which the transplantation of BMMSCs improves cognitive and behavioral deficits in AD models.Gene expression profile can be utilized to establish statistical regression model for the evaluation of therapeutic effect.The transplantation of autologous BMMSCs maybe a prospective therapy for patients with Alzheimer’s disease.

关键词： Alzheimer's disease Bone marrow mesenchymal stem cells Meta-analysis Amyloid P peptide Memory loss Cognitive deficits Animal model Neuropathology

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Bone marrow mesenchymal stem cells with Nogo-66 receptor gene silencing for repair of spinal cord injury

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Neural Regeneration Research 2014年第8期9卷 806-814页

作者： Zhiyuan Li Zhanxiu Zhang Lili Zhao Hui Li Suxia Wang Yong Shen Department of Joint Orthopedics Hebei Provincial Xingtai People’s Hospital Department of Spinal Orthopedics Third Hospital of Hebei Medical University

We hypothesized that RNA interference to silence Nogo-66 receptor gene expression in Bone marrow mesenchymal stem cells before transplantation might further improve neurological function in rats with spinal cord transection injury. After 2 weeks, the number of neurons and BrdU-positive cells in the Nogo-66 receptor gene silencing group was higher than in the bone marrow mesenchymal stem cell group, and significantly greater compared with the model group. After 4 weeks, behavioral performance was signiifcantly enhanced in the model group. Af-ter 8 weeks, the number of horseradish peroxidase-labeled nerve ifbers was higher in the Nogo-66 receptor gene silencing group than in the bone marrow mesenchymal stem cell group, and signiifcantly higher than in the model group. The newly formed nerve ifbers and myelinated ner ve ifbers were detectable in the central transverse plane section in the bone marrow mesenchymal stem cell group and in the Nogo-66 receptor gene silencing group.

关键词： nerve regeneration spinal cord injury Bone marrow mesenchymal stem cells Nogo-66receptor RNA interference horseradish peroxidase BrdU gene silencing neural regeneration

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Small extracellular vesicles from hypoxia-preconditioned Bone marrow mesenchymal stem cells attenuate spinal cord injury via miR-146a-5p-mediated regulation of macrophage polarization

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Neural Regeneration Research 2024年第10期19卷 2259-2269页

作者： Zeyan Liang Zhelun Yang Haishu Xie Jian Rao Xiongjie Xu Yike Lin Chunhua Wang Chunmei Chen Department of Neurosurgery Fujian Medical University Union HospitalFuzhouFujian ProvinceChina Fujian Neurosurgical Institute FuzhouFujian ProvinceChina

Spinal cord injury is a disabling condition with limited treatment options.Multiple studies have provided evidence suggesting that small extracellular vesicles(SEVs)secreted by Bone marrow mesenchymal stem cells(MSCs)help mediate the beneficial effects conferred by MSC transplantation following spinal cord injury.Strikingly,hypoxia-preconditioned bone marrow mesenchymal stem cell-derived SEVs(HSEVs)exhibit increased therapeutic potency.We thus explored the role of HSEVs in macrophage immune regulation after spinal cord injury in rats and their significance in spinal cord repair.SEVs or HSEVs were isolated from bone marrow MSC supernatants by density gradient ultracentrifugation.HSEV administration to rats via tail vein injection after spinal cord injury reduced the lesion area and attenuated spinal cord inflammation.HSEVs regulate macrophage polarization towards the M2 phenotype in vivo and in vitro.Micro RNA sequencing and bioinformatics analyses of SEVs and HSEVs revealed that mi R-146a-5p is a potent mediator of macrophage polarization that targets interleukin-1 receptor-associated kinase 1.Reducing mi R-146a-5p expression in HSEVs partially attenuated macrophage polarization.Our data suggest that HSEVs attenuate spinal cord inflammation and injury in rats by transporting mi R-146a-5p,which alters macrophage polarization.This study provides new insights into the application of HSEVs as a therapeutic tool for spinal cord injury.

关键词： Bone marrow mesenchymal stem cells hypoxia preconditioning interleukin-1 receptor-associated kinase 1 macrophages mesenchymal stem cells small extracellular vesicles spinal cord injury

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