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

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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Calcitonin gene related peptide modified mesenchymal stem cells reduce restenosis after carotid balloon injury in rats

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BIOCELL 2022年第8期46卷 1903-1909页

作者： PANKE CHEN SHUAI MA Department of Cardiology Affiliated Hospital of Zunyi Medical UniversityZunyi563003China

This work aimed to investigate the effects of calcitonin gene-related peptide(CGRP)-modified mesenchymal stem cells(MSCs)on vascular stenosis in carotid balloon-injured rats.The CGRP gene labeled with EGFP was transfected into bone marrow MSCs,and CGRP protein expression in MSCs was confirmed by immunofluorescence assays.A rat carotid balloon injury model was established using a surgicalmethod.CGRP-modifiedMSCs were orthotopically transplanted into the injured area of the rats.At 28 days after cell transplantation,EGFP and CD31 expression was detected by immunofluorescence staining.Hematoxylin-eosin(H&E)staining was used to detect the intima/media area of the injured carotid artery stenosis site,and the expression of proliferating cell nuclear antigen(PCNA)was detected by immunohistochemistry.MSCs from rat bone marrow positively expressed CD29 and negatively expressed CD45.In vivo immunofluorescence staining showed that EGFP expression was significantly increased at the vascular injury site of rats transplanted with MSC_CGRP compared with the control group on the 28th day after cell transplantation and that the damaged vessels exhibited continuous CD31 expression.H&E staining showed that the vascular intimal proliferation area of rats transplanted with MSC_CGRP was significantly reduced compared with that of other groups.Furthermore,the immunohistochemistry results showed that PCNA expression in the endothelium of the MSC_CGRP group was lower than that of the other groups.Therefore,MSCs transfected with the CGRP gene can express the CGRP protein,and the implantation of CGRPmodified MSCs at the damaged site after carotid balloon-induced injury can reduce the neointimal area.

关键词： Mesenchymal stem cells Calcitonin gene-related peptide lentiviral transfection Cell transplantation Restenosis

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The study on neural stem cells by Lentivirus mediated UCP2 lower expression

The study on neural stem cells by Lentivirus mediated UCP2 l...

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第八届泛环渤海生物化学与分子生物学会2018年学术交流...

作者： Kai-li Zhang Hujun Jin-rong Suo Zhi-zhen Liu Department of Biochemistry and Molecular Biology Shanxi Medical University

Objectives:1. Isolation, cultivation and identify C57 mice primary neural stem cells, providing a cell model to study the mechanism of neural tube defects caused by low expression of UCP2. 2. Construct an effective UCP2 RNA interference vector, and establish an efficient method to transfect neural stem cells, to support the study of gene function latter.3. Testing the change of ROS level and cell apoptosis after UCP2 experssion decrease in NSCs, exploring the pathogenesis of NTDs caused by UCP2 lower expression. Methods:1. Neural stem cells extraction, cultivation and identification: Through mechanical method, isolating neural stem cells from 14.5 days fetal rat’s brain tissue, Neural stem cells were identified by characteristic protein nestin immunofluorescence staining. DMEM/F12 culture medium containing 10% fetal calf serum was used to induce NSCs to differentiate, neuron, astrocyte and oligodendroglia were identified through characteristic proteins NF-H, GFAP and GALC immunofluorescence staining. 2. Construct UCP2 RNA interfere lentiviral vector and virus packing: Targeting UCP2 gene specific sequence were designed to link with p Magic4.1 lentiviral vector(p NL-EGFP/CMV/WPREdU 3-sh mU CP2). Then virus packing recombinant lentiviral vectors were harvested from 293 T cells with recombinant lentiviral vector, second generation virus packing plasmid p CD/NL-BH*DDD and membrane protein expression plasmid p LTR-G co-transfection.3. Construct electroporation UCP2 RNA interfere vector: The same as UCP2 RNA interfere lentiviral vector p NL-EGFP/CMV/WPREdU 3-sh mU CP2 above.4. Compare lentiviral transfection and electroporation: NSCs were transfected by lentiviral transfection and electroporation, transfection efficiency was compared By observing the green fluorescent protein expression of NSCs;The interference maintenance time was compared by green fluorescent intensity of NSCs after transfection 48 h and 72 h. Western Blot and QPCR were used to test NSCs UCP2 expression after lentiviral transfection. 5. ROS level det

关键词： neural stem cells uncoupling protein 2 lentiviral transfection reactive oxygen species cell apoptosis

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Study on Neural stem cells by Lentivirus mediated UCP2 lower expression

Study on Neural stem cells by Lentivirus mediated UCP2 lower...

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2017第七届泛环渤海生物化学与分子生物学会学术交流会

作者： Kai-li Zhang San-san Jia Jin-rong Suo Zhi-zhen Liu Jun Xie Department of Biochemistry and Molecular Biology Shanxi Medical University

Objectives:1.Isolation,cultivation and identify C57 mice primary neural stem cells,providing a cell model to study the mechanism of neural tube defects caused by low expression of UCP2.2.Construct an effective UCP2 RNA interference vector,and establish an efficient method to transfect neural stem cells,to support the study of gene function latter.3.Testing the change of ROS level and cell apoptosis after UCP2 experssion decrease in NSCs,exploring the pathogenesis of NTDs caused by UCP2 lower expression.4.Testing the change of ROS level and cell apoptosis after UCP2 experssion decrease in NSCs,exploring the pathogenesis of NTDs caused by UCP2 lower expression.Methods:1.Neural stem cells extraction,cultivation and identification.2.Construct UCP2 RNA interfere lentiviral vector and virus packing.***.lentiviral transfection:Western Blot and QPCR were used to test NSCs UCP2expression after lentiviral transfection.4.ROS level detection:Testing NSCs ROS level of blank group,negative control group and UCP2 low expression vector transfection experimental group by DCFH-DA respectively,Comparing ROS level of each group.5.Cells apoptosis detection:Dividing NSCs into three groups:blank group,negative control group and UCP2 low expression vector transfection experimental group.Caspase3 activation fluorescent staining was used to test the rate of caspase3 activation NSCs,Western Blot was used to test caspase3 expression.6.The mechanism of UCP2 and ROS production and apoptosis was further explored.

关键词： neural stem cells uncoupling protein 2 lentiviral transfection reactive oxygen species cell apoptosis

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