检索结果-南通市图书馆

Essential role of MALAT1 in reducing traumatic brain injury

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Neural Regeneration Research 2022年第8期17卷 1776-1784页

作者： Na Wu Chong-Jie Cheng Jian-Jun Zhong Jun-Chi He Zhao-Si Zhang Zhi-Gang Wang Xiao-Chuan Sun Han Liu Department of Neurosurgery the First Affiliated Hospital of Chongqing Medical UniversityChongqingChina Department of Neurosurgery Qilu Hospital of Shandong University(Qingdao Campus)QingdaoShandong ProvinceChina

As a highly evolutionary conserved long non-coding RNA,metastasis associated lung adenocarcinoma transcript 1(MALAT1)was first demonstrated to be related to lung tumor metastasis by promoting angiogenesis.To investigate the role of MALAT1 in traumatic brain injury,we established mouse models of controlled cortical impact and cell models of oxygen-glucose deprivation to mimic traumatic brain injury in vitro and in vivo.The results revealed that MALAT1 silencing in vitro inhibited endothelial cell viability and tube formation but increased migration.In MALAT1-deficient mice,endothelial cell proliferation in the injured cortex,functional vessel density and cerebral blood flow were reduced.Bioinformatic analyses and RNA pull-down assays validated enhancer of zeste homolog 2(EZH2)as a downstream factor of MALAT1 in endothelial cells.Jagged-1,the Notch homolog 1(NOTCH1)agonist,reversed the MALAT1 deficiency-mediated impairment of angiogenesis.Taken together,our results suggest that MALAT1 controls the key processes of angiogenesis following traumatic brain injury in an EZH2/NOTCH1-dependent manner.

关键词： angiogenesis controlled cortical impact EZH2 Jagged-1 LncRNA MALAT1 NOTCH1 oxygen-glucose deprivation traumatic brain injury vascular remodeling

Identification of predictive MRI and functional biomarkers in a pediatric piglet traumatic brain injury model

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2021年第2期16卷 338-344页

作者： Hongzhi Wang Emily W.Baker Abhyuday Mandal Ramana M.Pidaparti Franklin D.West Holly A.Kinder Department of Statistics University of GeorgiaAthensGAUSA Regenerative Bioscience Center University of GeorgiaAthensGAUSA Department of Animal and Dairy Science University of GeorgiaAthensGAUSA College of Engineering University of GeorgiaAthensGAUSA

Traumatic brain injury(TBI) at a young age can lead to the development of long-term functional impairments. Severity of injury is well demonstrated to have a strong influence on the extent of functional impairments;however, identification of specific magnetic resonance imaging(MRI) biomarkers that are most reflective of injury severity and functional prognosis remain elusive. Therefore, the objective of this study was to utilize advanced statistical approaches to identify clinically relevant MRI biomarkers and predict functional outcomes using MRI metrics in a translational large animal piglet TBI model. TBI was induced via controlled cortical impact and multiparametric MRI was performed at 24 hours and 12 weeks post-TBI using T1-weighted, T2-weighted, T2-weighted fluid attenuated inversion recovery, diffusion-weighted imaging, and diffusion tensor imaging. Changes in spatiotemporal gait parameters were also assessed using an automated gait mat at 24 hours and 12 weeks post-TBI. Principal component analysis was performed to determine the MRI metrics and spatiotemporal gait parameters that explain the largest sources of variation within the datasets. We found that linear combinations of lesion size and midline shift acquired using T2-weighted imaging explained most of the variability of the data at both 24 hours and 12 weeks post-TBI. In addition, linear combinations of velocity, cadence, and stride length were found to explain most of the gait data variability at 24 hours and 12 weeks post-TBI. Linear regression analysis was performed to determine if MRI metrics are predictive of changes in gait. We found that both lesion size and midline shift are significantly correlated with decreases in stride and step length. These results from this study provide an important first step at identifying relevant MRI and functional biomarkers that are predictive of functional outcomes in a clinically relevant piglet TBI model. This study was approved by the University of Georgia Institutional Animal Care and Use Committee(AUP:

关键词： controlled cortical impact gait analysis linear regression magnetic resonance imaging motor function pediatric pig model principal component analysis traumatic brain injury

Temporal changes in inflammatory mitochondria-enriched microRNAs following traumatic brain injury and effects of miR-146a nanoparticle delivery

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2021年第3期16卷 514-522页

作者： Wang-Xia Wang Paresh Prajapati Hemendra J.Vekaria Malinda Spry Amber L.Cloud Patrick G.Sullivan Joe E.Springer Sanders Brown Center on Aging University of KentuckyLexingtonKYUSA Spinal Cord and Brain Injury Research Center University of KentuckyLexingtonKYUSA Department of Pathology&Laboratory Medicine University of KentuckyLexingtonKYUSA Department of Neuroscience University of KentuckyLexingtonKYUSA

MicroRNAs(miRNAs)are small non-coding RNA molecules that regulate post-transcriptional gene expression and contribute to all aspects of cellular function.We previously reported that the activities of several mitochondria-enriched miRNAs regulating inflammation(i.e.,miR-142-3p,miR-142-5p,and miR-146a)are altered in the hippocampus at 3–12 hours following a severe traumatic brain injury.In the present study,we investigated the temporal expression profile of these inflammatory miRNAs in mitochondria and cytosol fractions at more chronic post-injury times following severe controlled cortical impact injury in rats.In addition,several inflammatory genes were analyzed in the cytosol fractions.The analysis showed that while elevated levels were observed in cytoplasm,the mitochondria-enriched miRNAs,miR-142-3p and miR-142-5p continued to be significantly reduced in mitochondria from injured hippocampi for at least 3 days and returned to near normal levels at 7 days post-injury.Although not statistically significant,miR-146a also remained at reduced levels for up to 3 days following controlled cortical impact injury,and recovered by 7 days.In contrast,miRNAs that are not enriched in mitochondria,including miR-124a,miR-150,miR-19b,miR-155,and miR-223 were either increased or demonstrated no change in their levels in mitochondrial fractions for 7 days.The one exception was that miR-223 levels were reduced in mitochondria at 1 day following injury.No major alterations were observed in sham operated animals.This temporal pattern was unique to mitochondria-enriched miRNAs and correlated with injury-induced changes in mitochondrial bioenergetics as well as expression levels of several inflammatory markers.These observations suggested a potential compartmental re-distribution of the mitochondria-enriched inflammatory miRNAs and may reflect an intracellular mechanism by which specific miRNAs regulate injury-induced inflammatory signaling.To test this,we utilized a novel peptide-based nanoparticle strategy for in vitro and in vivo

关键词： cell permeable peptide-delivery controlled cortical impact inflammatory pathway mitochondria-associated microRNA nanoparticle nuclear factor-kappa B traumatic brain injury

Automated monitoring of early neurobehavioral changes in mice following traumatic brain injury

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2016年第2期11卷 248-256页

作者： Wenrui Qu Nai-kui Liu Xin-min (Simon) Xie Rui Li Xiao-ming Xu Hand & Foot Surgery and Reparative & Reconstructive Surgery Center Orthopaedic Hospital of the Second Hospital of Jilin UniversityChangchun Jilin Province China Spinal Cord and Brain Injury Research Group Stark Neurosciences Research Institute Indiana University School of Medicine Indianapolis IN USA Department of Neurological Surgery Indiana University School of Medicine Indianapolis IN USA Department of Anatomy and Cell Biology Indiana University School of Medicine Inclianapolis IN USA Goodman Campbell Brain and Spine Inctianapolis IN USA AfaSci Research Laboratories Redwood City CA USA

Traumatic brain injury often causes a variety of behavioral and emotional impairments that can develop into chronic disorders. Therefore, there is a need to shift towards identifying early symptoms that can aid in the prediction of traumatic brain injury outcomes and behavioral endpoints in patients with traumatic brain injury after early interventions. In this study, we used the Smart Cage system, an automated quantitative approach to assess behavior alterations in mice during an early phase of traumatic brain injury in their home cages. Female C57BL/6 adult mice were subjected to moderate controlled cortical impact（CCI） injury. The mice then received a battery of behavioral assessments including neurological score, locomotor activity, sleep/wake states, and anxiety-like behaviors on days 1, 2, and 7 after CCI. Histological analysis was performed on day 7 after the last assessment. Spontaneous activities on days 1 and 2 after injury were significantly decreased in the CCI group. The average percentage of sleep time spent in both dark and light cycles were significantly higher in the CCI group than in the sham group. For anxiety-like behaviors, the time spent in a light compartment and the number of transitions between the dark/light compartments were all significantly reduced in the CCI group than in the sham group. In addition, the mice suffering from CCI exhibited a preference of staying in the dark compartment of a dark/light cage. The CCI mice showed reduced neurological score and histological abnormalities, which are well correlated to the automated behavioral assessments. Our findings demonstrate that the automated Smart Cage system provides sensitive and objective measures for early behavior changes in mice following traumatic brain injury.

关键词： nerve regeneration traumatic brain injury controlled cortical impact automated behavior motor activity anxiety exploratoryactivity sleep neural regeneration

Endorepellin downregulation promotes angiogenesis after experimental traumatic brain injury

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2024年第5期19卷 1092-1097页

作者： Qian Zhang Yao Jing Qiuyuan Gong Lin Cai Ren Wang Dianxu Yang Liping Wang Meijie Qu Hao Chen Yaohui Tang Hengli Tian Jun Ding Zhiming Xu Department of Gerontology Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghaiChina Department of Neurosurgery Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghaiChina Department of Neurology Renji HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghaiChina School of Biomedical Engineering and Med-X Research Institute Shanghai Jiao Tong UniversityShanghaiChina Department of Neurology Affiliated Hospital of Qingdao UniversityQingdaoShandong ProvinceChina

Endorepellin plays a key role in the regulation of angiogenesis,but its effects on angiogenesis after traumatic brain injury are unclear.This study explored the effects of endorepellin on angiogenesis and neurobehavioral outcomes after traumatic brain injury in mice.Mice were randomly divided into four groups:sham,controlled cortical impact only,adeno-associated virus(AAV)-green fluorescent protein,and AAV-shEndorepellin-green fluorescent protein groups.In the controlled cortical impact model,the transduction of AAV-shEndorepellin-green fluorescent protein downregulated endorepellin while increasing the number of CD31+/Ki-67+proliferating endothelial cells and the functional microvessel density in mouse brain.These changes resulted in improved neurological function compared with controlled cortical impact mice.Western blotting revealed increased expression of vascular endothelial growth factor and angiopoietin-1 in mice treated with AAV-shEndorepellin-green fluorescent protein.Synchrotron radiation angiography showed that endorepellin downregulation promoted angiogenesis and increased cortical neovascularization,which may further improve neurobehavioral outcomes.Furthermore,an in vitro study showed that downregulation of endorepellin increased tube formation by human umbilical vein endothelial cells compared with a control.Mechanistic analysis found that endorepellin downregulation may mediate angiogenesis by activating vascular endothelial growth factor-and angiopoietin-1-related signaling pathways.

关键词： angiogenesis controlled cortical impact endorepellin neurological function traumatic brain injury