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南京医科大学学报(自然科学版)                                  第42卷第6期
               ·780 ·                     Journal of Nanjing Medical University(Natural Sciences)   2022年6月


             ·基础研究·

              小鼠脊髓损伤后Bmi⁃1在脊髓中的表达变化



              金瑶瑶 ,赵伟华 ,高 钰 ,肖晨宇 ,张永杰                  1,2*
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               南京医科大学人体解剖学系,衰老及相关疾病研究重点实验室,江苏                        南京    211166;南京中医药大学附属常州市中医医院
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              骨科,江苏 常州       213003;南京医科大学第一临床医学院,江苏              南京 211166
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             [摘    要] 目的:检测小鼠脊髓损伤(spinal cord injury,SCI)后 B 淋巴瘤 Mo⁃MLV 插入区 1(B cell⁃specific MLV integration site⁃
              1,Bmi⁃1)在脊髓中的表达变化。方法:取2月龄C57Bl/6小鼠,利用LISA脊髓损伤造模仪制作小鼠第9胸椎节段(T9)中度脊髓
              钝挫伤模型,通过免疫荧光染色与 Western blot 检测,初步观察 SCI 后 1、3、7、14、28 d 时 Bmi⁃1 在脊髓中的表达变化与细胞定
              位。结果:Bmi⁃1在脊髓中的表达,于损伤后1 d即上调并达峰值,至损伤后28 d仍保持较高水平,其表达变化与增殖细胞核抗
              原(proliferating cell nuclear antigen,PCNA)的表达变化趋势一致。免疫荧光染色结果显示:SCI后,Bmi⁃1与离子钙接头蛋白分
              子1(ionized calcium binding adapter molecule 1,Iba⁃1)、髓鞘碱性蛋白(myelin basic protein,MBP)、神经元核心抗原(neuronal nu⁃
              clei antigen,NeuN)及血小板内皮细胞黏附分子1(platelet and endothelial cell adhesion molecule⁃1,PECAM⁃1/CD31)共表达;Bmi⁃1
              与神经胶质纤维酸性蛋白(glial fibrillary acidic protein,GFAP)无共表达。结论:小鼠脊髓损伤后脊髓中Bmi⁃1表达上调,主要定位
              于小胶质细胞、髓鞘细胞、神经元与血管内皮细胞,且在小胶质细胞中的表达尤为显著。提示Bmi⁃1在脊髓损伤后的表达变化可
              能与小胶质细胞的增殖与活化、内源性髓鞘再生及血管内皮细胞的活化有关,可能在脊髓损伤后的病理过程中具有重要意义。
             [关键词] 脊髓损伤;Bmi⁃1;细胞定位;小鼠
             [中图分类号] R651.2                   [文献标志码] A                        [文章编号] 1007⁃4368(2022)06⁃780⁃10
              doi:10.7655/NYDXBNS20220603


              Expression of Bmi⁃1 in spinal cord after mice spinal cord injury

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              JIN Yaoyao ,ZHAO Weihua ,GAO Yu ,XIAO Chenyu ,ZHANG Yongjie    1,2*
              1 Department of Human Anatomy,Key Laboratory for Aging & Diseases,Nanjing Medical University,Nanjing
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              211166;Department of Orthopaedics,the Affiliated Changzhou Hospital of Traditional Chinese Medicine,Nanjing
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              University of Chinese Medicine,Changzhou 213003; the First Clinical Medical College,Nanjing Medical
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              University,Nanjing 211166,China
             [Abstract] Objective:This study aims to explore the expression of B cell⁃specific MLV integration site⁃1(Bmi⁃1)in mice spinal
              cord after spinal cord injury(SCI). Methods:Two month ⁃ old C57Bl/6 mice received moderate contusion SCI at T9 using LISA
              impactor. The expression and cellular localization of Bmi⁃1 in spinal cord at the day of 1,3,7,14 and 28 post SCI were detected by
              Western blot and immunofluorescence staining. Results:The results of Western blot showed that the expression of Bmi ⁃ 1 was
              increased and achieved a peak value at day one post SCI,and which was higher than normal till to the day 28 post SCI. The tendency of
              the Bmi ⁃ 1 expression was consistent with the expression of proliferating cell nuclear antigen(PCNA). The results of the
              immunofluorescence staining showed that the Bmi⁃1 was increased and co⁃localized with ionized calcium binding adapter molecule 1
             (Iba⁃1),myelin basic protein(MBP),neuronal nuclei antigen(NeuN),and platelet and endothelial cell adhesion molecule⁃1(PECAM⁃1/
              yCD31),but which was not co⁃localized with glial fibrillary acidic protein(GFAP)after SCI. Conclusion:The expression of Bmi⁃1 was
              increased and mainly localized in microglia,myelin cells,neuron and endothelium,and especially in microglia after SCI. It suggests
              that the expression of Bmi⁃1 may relate with the proliferation and activation of microglia,the endogenous remyelination,and the activity
              of the endothelium. The Bmi⁃1 may involve in the pathological process after SCI.
             [Key words] spinal cord injury;Bmi⁃1;cellular localization;mice
                                                                            [J Nanjing Med Univ,2022,42(06):780⁃789]
             [基金项目] 国家自然科学基金(81472081);2020年江苏省青蓝工程资助项目
              ∗
              通信作者(Corresponding author),E⁃mail:zhangyongjie@njmu.edu.cn
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