Krüppel-like factor 7 attenuates hippocampal neuronal injury after traumatic brain injury
Krüppel-like factor 7 attenuates hippocampal neuronal injury after traumatic brain injury作者机构:Institute of Neural Tissue EngineeringMudanjiang Medical UniversityMudanjiangHeilongjiang ProvinceChina Department of AnatomyCollege of Basic Medical SciencesChengde Medical UniversityChengdeHebei ProvinceChina Hebei Key Laboratory of Nerve Injury and RepairChengde Medical UniversityChengdeHebei ProvinceChina Department of OtorhinolaryngologyMudanjiang City Second People’s HospitalMudanjiangHeilongjiang ProvinceChina The First Department of General SurgeryHongqi HospitalMudanjiang Medical UniversityMudanjiangHeilongjiang ProvinceChina
出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))
年 卷 期:2022年第17卷第3期
页 面:661-672页
核心收录:
学科分类:1002[医学-临床医学] 1010[医学-医学技术(可授医学、理学学位)] 100215[医学-康复医学与理疗学] 100204[医学-神经病学] 10[医学]
基 金:supported by the National Natural Science Foundation of China,No.81870977 (to YW) the Natural Science Foundation of Heilongjiang of China,No.H2018068 (to WYL) the Basic Research Operating Expenses Program of Heilongjiang Provincial Universities of China,No.2019-KYYWFMY-0018 (to WYL) the Graduate Innovative Research Projects of Mudanjiang Medical College of China,No.YJSCX-MY22 (to DM) Key projects of Education Department of Hebei Province of China,No.ZD2020178 (to XMF) Hebei Key Laboratory of Nerve Injury and Repair of China (to XMF)
主 题:apoptosis hippocampus JAK2/STAT3 Kruppel-like factor 7 neuroprotection oxygen-glucose deprivation stretch traumatic brain injury
摘 要:Our previous study has shown that the transcription factor Krüppel-like factor 7(KLF7) promotes peripheral nerve regeneration and motor function recovery after spinal cord ***7 also participates in traumatic brain injury,but its regulatory mechanisms remain poorly *** the present study,an HT22 cell model of traumatic brain injury was established by stretch injury and oxygenglucose *** cells were then transfected with an adeno-associated virus carrying KLF7(AAV-KLF7).The results revealed that,after stretch injury and oxygen-glucose deprivation,KLF7 greatly reduced apoptosis,activated caspase-3 and lactate dehydrogenase,downregulated the expression of the apoptotic markers B-cell lymphoma 2(Bcl-2)-associated X protein(Bax) and cleaved caspase-3,and increased the expression of βIII-tubulin and the antiapoptotic marker ***,KLF7 overexpression upregulated Janus kinase 2(JAK2) and signal transducer and activator of transcription 3(STAT3) phosphorylation in HT22 cells treated by stretch injury and oxygenglucose *** assays revealed that KLF7 directly participated in the phosphorylation of *** addition,treatment with AG490,a selective inhibitor of JAK2/STAT3,weakened the protective effects of KLF7.A mouse controlled cortical impact model of traumatic brain injury was then *** 30 minutes before modeling,AAV-KLF7 was injected into the ipsilateral lateral *** protein and m RNA levels of KLF7 in the hippocampus were increased at 1 day after injury and recovered to normal levels at 3 days after ***7 reduced ipsilateral hippocampal atrophy,decreased the injured cortex volume,downregulated Bax and cleaved caspase-3 expression,and increased the number of 5-bromo-2 -deoxyuridine-positive neurons and Bcl-2 protein ***,KLF7 transfection greatly enhanced the phosphorylation of JAK2 and STAT3 in the ipsilateral *** results suggest that KLF7 may protect h