[目的]探究FNDC5在前列腺癌中的表达及其对前列腺癌DU145细胞增殖和转移的影响。[方法]通过免疫组化分析FNDC5在前列腺癌组织的表达,将前列腺癌DU145细胞分为3个实验组:阴性对照组、si FNDC5组、LY294002组。通过CCK-8实验与EdU染色分析...[目的]探究FNDC5在前列腺癌中的表达及其对前列腺癌DU145细胞增殖和转移的影响。[方法]通过免疫组化分析FNDC5在前列腺癌组织的表达,将前列腺癌DU145细胞分为3个实验组:阴性对照组、si FNDC5组、LY294002组。通过CCK-8实验与EdU染色分析DU145细胞的增殖活性;通过细胞划痕实验分析DU145细胞的迁移能力;通过Transwell实验分析DU145细胞的侵袭能力;通过蛋白免疫印迹实验分析DU145细胞中PI3K、AKT蛋白的表达水平。[结果]FNDC5在前列腺癌组织中表达上调(18.25%±2.15%vs 69.69%±5.97%;P<0.05)。与阴性对照组比较,si FNDC5以及LY294002组的DU145细胞增殖能力下降(2.63±0.26 vs 1.53±0.12 vs 1.51±0.17;P<0.05);si FNDC5以及LY294002组的DU145细胞的迁移、侵袭能力下降(73.68±5.62 vs 38.81±3.56 vs 39.21±5.77;P<0.05);si FNDC5以及LY294002组的DU145细胞PI3K、AKT蛋白表达水平降低(0.79±0.07 vs 0.33±0.09 vs 0.32±0.08;0.85±0.02 vs 0.31±0.07 vs 0.35±0.03;P<0.05)。[结论]FNDC5在前列腺癌组织中表达增加。抑制FNDC5表达后,前列腺癌DU145细胞的增殖活性、迁移与侵袭能力降低,该作用与FNDC5调节PI3K/AKT信号通路相关。展开更多
Background: Aging-induced cardiac hypertrophy and reduced skeletal muscle strength contribute to increased disease risk and life burden in the elderly. FNDC5 acts as a protective muscle factor in both cardiac and skel...Background: Aging-induced cardiac hypertrophy and reduced skeletal muscle strength contribute to increased disease risk and life burden in the elderly. FNDC5 acts as a protective muscle factor in both cardiac and skeletal muscle. This study aims to examine the relationship between cardiac FNDC5 and aging-related cardiac hypertrophy and decreased skeletal muscle strength. Methods: Male young C57BL/6 mice (5 months old, n = 6) and aged mice (21 months old, n = 6) were utilized in the study and housed in a specific pathogen-free (SPF) environment. Prior to the experiment, grip strength tests were performed on the mice, and heart tissues were collected for morphological analysis, including the assessment of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) and fibronectin type III-containing structural domain 5 (FNDC5) protein levels. Furthermore, myosin heavy chain II (MyHC II), skeletal muscle-specific transcription factor (MyoD), muscle RING-finger protein-1 (MuRF1), and FNDC5 levels were evaluated in the quadriceps muscle. The correlations between heart weight and FNDC5 expression levels, as well as skeletal muscle indices in the mice, were subsequently analyzed. Result: Aging leads to cardiac hypertrophy and reduced expression of PGC-1α and FNDC5 proteins. Concurrently, there is a decline in the strength of skeletal muscle, along with decreased expression of MyHC II and increased expression of MURF1 and MyoD. Correlation analysis demonstrated strong positive associations between myocardial FNDC5 protein levels and limb grip strength, as well as MyHC II, and strong negative associations with MyoD and MuRF1. Conclusion: There may be a significant association between aging-induced cardiac hypertrophy and decreased skeletal muscle strength, with FNDC5 potentially playing a crucial role as a regulatory molecule facilitating communication between the heart and skeletal muscle.展开更多
Cognitive dysfunction often occurs in Alzheimer’s disease,Parkinson’s disease,cerebrovascular disease,or other neurodegenerative diseases,and can significantly impact the life quality of patients and create serious ...Cognitive dysfunction often occurs in Alzheimer’s disease,Parkinson’s disease,cerebrovascular disease,or other neurodegenerative diseases,and can significantly impact the life quality of patients and create serious social,psychological,and economic burdens for individuals and their families.Numerous studies have confirmed that exercise can slow the decline in cognitive function through multiple pathways,in which fibronectin type III domain-containing protein 5(FNDC5)plays an important role.However,the current research on the modulation of FNDC5 by exercise and its ability to improve hippocampal cognitive function lacks a systematic and comprehensive understanding.Therefore,this review focuses on the latest research progress regarding the role of exercise-induced FNDC5 in cognitive function,systematically reviews the positive effects of FNDC5 on cognitive function impairment caused by various factors,and clarifies the specific mechanisms by which exerciseinduced FNDC5 improves cognitive function by inhibiting neuroinflammation and improving hippocampal neurogenesis and hippocampal synaptic plasticity.Based on the existing literature,we also identify the areas that require further research in this field.Overall,this review provides a theoretical basis for exercise-based prevention and improvement of cognitive function impairment.展开更多
文摘[目的]探究FNDC5在前列腺癌中的表达及其对前列腺癌DU145细胞增殖和转移的影响。[方法]通过免疫组化分析FNDC5在前列腺癌组织的表达,将前列腺癌DU145细胞分为3个实验组:阴性对照组、si FNDC5组、LY294002组。通过CCK-8实验与EdU染色分析DU145细胞的增殖活性;通过细胞划痕实验分析DU145细胞的迁移能力;通过Transwell实验分析DU145细胞的侵袭能力;通过蛋白免疫印迹实验分析DU145细胞中PI3K、AKT蛋白的表达水平。[结果]FNDC5在前列腺癌组织中表达上调(18.25%±2.15%vs 69.69%±5.97%;P<0.05)。与阴性对照组比较,si FNDC5以及LY294002组的DU145细胞增殖能力下降(2.63±0.26 vs 1.53±0.12 vs 1.51±0.17;P<0.05);si FNDC5以及LY294002组的DU145细胞的迁移、侵袭能力下降(73.68±5.62 vs 38.81±3.56 vs 39.21±5.77;P<0.05);si FNDC5以及LY294002组的DU145细胞PI3K、AKT蛋白表达水平降低(0.79±0.07 vs 0.33±0.09 vs 0.32±0.08;0.85±0.02 vs 0.31±0.07 vs 0.35±0.03;P<0.05)。[结论]FNDC5在前列腺癌组织中表达增加。抑制FNDC5表达后,前列腺癌DU145细胞的增殖活性、迁移与侵袭能力降低,该作用与FNDC5调节PI3K/AKT信号通路相关。
文摘Background: Aging-induced cardiac hypertrophy and reduced skeletal muscle strength contribute to increased disease risk and life burden in the elderly. FNDC5 acts as a protective muscle factor in both cardiac and skeletal muscle. This study aims to examine the relationship between cardiac FNDC5 and aging-related cardiac hypertrophy and decreased skeletal muscle strength. Methods: Male young C57BL/6 mice (5 months old, n = 6) and aged mice (21 months old, n = 6) were utilized in the study and housed in a specific pathogen-free (SPF) environment. Prior to the experiment, grip strength tests were performed on the mice, and heart tissues were collected for morphological analysis, including the assessment of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) and fibronectin type III-containing structural domain 5 (FNDC5) protein levels. Furthermore, myosin heavy chain II (MyHC II), skeletal muscle-specific transcription factor (MyoD), muscle RING-finger protein-1 (MuRF1), and FNDC5 levels were evaluated in the quadriceps muscle. The correlations between heart weight and FNDC5 expression levels, as well as skeletal muscle indices in the mice, were subsequently analyzed. Result: Aging leads to cardiac hypertrophy and reduced expression of PGC-1α and FNDC5 proteins. Concurrently, there is a decline in the strength of skeletal muscle, along with decreased expression of MyHC II and increased expression of MURF1 and MyoD. Correlation analysis demonstrated strong positive associations between myocardial FNDC5 protein levels and limb grip strength, as well as MyHC II, and strong negative associations with MyoD and MuRF1. Conclusion: There may be a significant association between aging-induced cardiac hypertrophy and decreased skeletal muscle strength, with FNDC5 potentially playing a crucial role as a regulatory molecule facilitating communication between the heart and skeletal muscle.
基金supported by the Beijing Natural Science Foundation(No.7222115)the Central University Basic Scientific Research Business Fee Project(No.2023073),China.
文摘Cognitive dysfunction often occurs in Alzheimer’s disease,Parkinson’s disease,cerebrovascular disease,or other neurodegenerative diseases,and can significantly impact the life quality of patients and create serious social,psychological,and economic burdens for individuals and their families.Numerous studies have confirmed that exercise can slow the decline in cognitive function through multiple pathways,in which fibronectin type III domain-containing protein 5(FNDC5)plays an important role.However,the current research on the modulation of FNDC5 by exercise and its ability to improve hippocampal cognitive function lacks a systematic and comprehensive understanding.Therefore,this review focuses on the latest research progress regarding the role of exercise-induced FNDC5 in cognitive function,systematically reviews the positive effects of FNDC5 on cognitive function impairment caused by various factors,and clarifies the specific mechanisms by which exerciseinduced FNDC5 improves cognitive function by inhibiting neuroinflammation and improving hippocampal neurogenesis and hippocampal synaptic plasticity.Based on the existing literature,we also identify the areas that require further research in this field.Overall,this review provides a theoretical basis for exercise-based prevention and improvement of cognitive function impairment.
