Vimentin is a major type Ⅲ intermediate filament protein that plays important roles in several basic cellular functions including cell migration, proliferation, and division. Although vimentin is a cytoplasmic protei...Vimentin is a major type Ⅲ intermediate filament protein that plays important roles in several basic cellular functions including cell migration, proliferation, and division. Although vimentin is a cytoplasmic protein, it also exists in the extracellular matrix and at the cell surface. Previous studies have shown that vimentin may exert multiple physiological effects in different nervous system injuries and diseases. For example, the studies of vimentin in spinal cord injury and stroke mainly focus on the formation of reactive astrocytes. Reduced glial scar, increased axonal regeneration, and improved motor function have been noted after spinal cord injury in vimentin and glial fibrillary acidic protein knockout(GFAPVIM) mice. However, attenuated glial scar formation in post-stroke in GFAP–/– VIM–/– mice resulted in abnormal neuronal network restoration and worse neurological recovery. These opposite results have been attributed to the multiple roles of glial scar in different temporal and spatial conditions. In addition, extracellular vimentin may be a neurotrophic factor that promotes axonal extension by interaction with the insulin-like growth factor 1 receptor. In the pathogenesis of bacterial meningitis, cell surface vimentin is a meningitis facilitator, acting as a receptor of multiple pathogenic bacteria, including E. coli K1, Listeria monocytogenes, and group B streptococcus. Compared with wild type mice, VIMmice are less susceptible to bacterial infection and exhibit a reduced inflammatory response, suggesting that vimentin is necessary to induce the pathogenesis of meningitis. Recently published literature showed that vimentin serves as a double-edged sword in the nervous system, regulating axonal regrowth, myelination, apoptosis, and neuroinflammation. This review aims to provide an overview of vimentin in spinal cord injury, stroke, bacterial meningitis, gliomas, and peripheral nerve injury and to discuss the potential therapeutic methods involving vimentin manipulation in improving axonal regeneration, alleviating infection, inhibiting brain tumor progression, and enhancing nerve myelination.展开更多
目的:探究益肾通癃汤对前列腺癌(PCa)皮下种植瘤模型裸鼠N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)表达的影响。方法:用前列腺癌PC-3细胞悬液建立PCa皮下种植瘤模型裸鼠,造模成功后将其随机分为模型组、益肾通癃汤低剂量组、益肾通...目的:探究益肾通癃汤对前列腺癌(PCa)皮下种植瘤模型裸鼠N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)表达的影响。方法:用前列腺癌PC-3细胞悬液建立PCa皮下种植瘤模型裸鼠,造模成功后将其随机分为模型组、益肾通癃汤低剂量组、益肾通癃汤中剂量组、益肾通癃汤高剂量组,每组10只。各给药组灌胃给予相应药物,模型组灌胃给予等体积生理盐水,2次/d,连续3周。给药结束后,观察裸鼠一般状态,测量体质量及瘤体大小,称重并计算抑瘤率;运用HE染色观察各组裸鼠种植瘤病理学改变;ELISA法检测各组裸鼠血清中N-cadherin、Vimentin的水平;Western blotting检测各组裸鼠种植瘤组织中N-cadherin、Vimentin蛋白表达情况;PCR检测各组裸鼠种植瘤组织中N-cadherin m RNA、Vimentin m RNA表达情况。结果:与模型组比较,益肾通癃汤低、中、高剂量组裸鼠状态均可,瘤体质量,血清中N-cadherin、Vimentin水平,种植瘤组织中N-cadherin、Vimentin的蛋白及m RNA相对表达量均降低(P<0.05),瘤体细胞少量坏死;与益肾通癃汤低剂量组比较,益肾通癃汤中、高剂量组裸鼠一般状态可,瘤体质量,血清中N-cadherin、Vimentin水平、种植瘤组织中N-cadherin、Vimentin蛋白及mRNA相对表达量均降低(P<0.05),瘤体细胞部分坏死;与益肾通癃汤中剂量组比较,益肾通癃汤高剂量组裸鼠一般状态良好,瘤体质量,血清中N-cadherin水平,种植瘤组织中N-cadherin、Vimentin蛋白相对表达量,种植瘤组织中Vimentin mRNA相对表达量均降低(P<0.05),瘤体细胞坏死多;益肾通癃汤高剂量组裸鼠血清中Vimentin水平、种植瘤组织中N-cadherin mRNA相对表达量与益肾通癃汤中剂量组比较,差异无统计学意义(P>0.05);益肾通癃汤低、中、高剂量组裸鼠抑瘤率分别为26.67%、42.45%、66.26%。结论:益肾通癃汤对人前列腺癌PC-3细胞皮下种植瘤模型裸鼠N-cadherin、Vimentin蛋白的表达具有一定的抑制作用,其机制可能与抑制肿瘤上皮间质转化(EMT)过程相关。展开更多
基金supported by the National Natural Science Foundation of China,No. 82071374Discipline Construction Project of Guangdong Medical University,Nos. 1.13 and 4.1.19+1 种基金College Students Innovative Experimental Project in Guangdong Medical University,Nos. FYDB015, ZCDS001, ZYDB004, ZYDB016, and ZZDI001College Students’ Science and Technology Innovation Training Project,Nos. GDMU2020194, GDMU2020195, GDMU2021021, GDMU2021023, GDMU2021091, GDMU2021111 (all to HFW)。
文摘Vimentin is a major type Ⅲ intermediate filament protein that plays important roles in several basic cellular functions including cell migration, proliferation, and division. Although vimentin is a cytoplasmic protein, it also exists in the extracellular matrix and at the cell surface. Previous studies have shown that vimentin may exert multiple physiological effects in different nervous system injuries and diseases. For example, the studies of vimentin in spinal cord injury and stroke mainly focus on the formation of reactive astrocytes. Reduced glial scar, increased axonal regeneration, and improved motor function have been noted after spinal cord injury in vimentin and glial fibrillary acidic protein knockout(GFAPVIM) mice. However, attenuated glial scar formation in post-stroke in GFAP–/– VIM–/– mice resulted in abnormal neuronal network restoration and worse neurological recovery. These opposite results have been attributed to the multiple roles of glial scar in different temporal and spatial conditions. In addition, extracellular vimentin may be a neurotrophic factor that promotes axonal extension by interaction with the insulin-like growth factor 1 receptor. In the pathogenesis of bacterial meningitis, cell surface vimentin is a meningitis facilitator, acting as a receptor of multiple pathogenic bacteria, including E. coli K1, Listeria monocytogenes, and group B streptococcus. Compared with wild type mice, VIMmice are less susceptible to bacterial infection and exhibit a reduced inflammatory response, suggesting that vimentin is necessary to induce the pathogenesis of meningitis. Recently published literature showed that vimentin serves as a double-edged sword in the nervous system, regulating axonal regrowth, myelination, apoptosis, and neuroinflammation. This review aims to provide an overview of vimentin in spinal cord injury, stroke, bacterial meningitis, gliomas, and peripheral nerve injury and to discuss the potential therapeutic methods involving vimentin manipulation in improving axonal regeneration, alleviating infection, inhibiting brain tumor progression, and enhancing nerve myelination.
文摘目的:探究益肾通癃汤对前列腺癌(PCa)皮下种植瘤模型裸鼠N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)表达的影响。方法:用前列腺癌PC-3细胞悬液建立PCa皮下种植瘤模型裸鼠,造模成功后将其随机分为模型组、益肾通癃汤低剂量组、益肾通癃汤中剂量组、益肾通癃汤高剂量组,每组10只。各给药组灌胃给予相应药物,模型组灌胃给予等体积生理盐水,2次/d,连续3周。给药结束后,观察裸鼠一般状态,测量体质量及瘤体大小,称重并计算抑瘤率;运用HE染色观察各组裸鼠种植瘤病理学改变;ELISA法检测各组裸鼠血清中N-cadherin、Vimentin的水平;Western blotting检测各组裸鼠种植瘤组织中N-cadherin、Vimentin蛋白表达情况;PCR检测各组裸鼠种植瘤组织中N-cadherin m RNA、Vimentin m RNA表达情况。结果:与模型组比较,益肾通癃汤低、中、高剂量组裸鼠状态均可,瘤体质量,血清中N-cadherin、Vimentin水平,种植瘤组织中N-cadherin、Vimentin的蛋白及m RNA相对表达量均降低(P<0.05),瘤体细胞少量坏死;与益肾通癃汤低剂量组比较,益肾通癃汤中、高剂量组裸鼠一般状态可,瘤体质量,血清中N-cadherin、Vimentin水平、种植瘤组织中N-cadherin、Vimentin蛋白及mRNA相对表达量均降低(P<0.05),瘤体细胞部分坏死;与益肾通癃汤中剂量组比较,益肾通癃汤高剂量组裸鼠一般状态良好,瘤体质量,血清中N-cadherin水平,种植瘤组织中N-cadherin、Vimentin蛋白相对表达量,种植瘤组织中Vimentin mRNA相对表达量均降低(P<0.05),瘤体细胞坏死多;益肾通癃汤高剂量组裸鼠血清中Vimentin水平、种植瘤组织中N-cadherin mRNA相对表达量与益肾通癃汤中剂量组比较,差异无统计学意义(P>0.05);益肾通癃汤低、中、高剂量组裸鼠抑瘤率分别为26.67%、42.45%、66.26%。结论:益肾通癃汤对人前列腺癌PC-3细胞皮下种植瘤模型裸鼠N-cadherin、Vimentin蛋白的表达具有一定的抑制作用,其机制可能与抑制肿瘤上皮间质转化(EMT)过程相关。
