小窝蛋白-1介导的信号通路在衰老中的作用
摘要
<正>随着社会的飞速发展,人口老龄化已成为世界各国的最终趋势~([1])。根据世界卫生组织的最新数据,预计到2050年,老年人口数目达到21亿~([2])。因此,如何在严峻的人口老龄化背景下,保障老年人的健康问题已成为当下的热门课题。小窝蛋白-1(Cav-1)介导的信号通路与衰老相关,了解其生物功能及其介导的信号通路可能为治疗衰老相关疾病提供潜在的治疗靶点。1 小窝及小窝蛋白家族小窝(Caveolae)是在细胞膜上特定的富含胆固醇和鞘磷脂的特殊脂
引文
[1] FEHLINGS M G, TETREAULT L,NATER A,et al.The aging of the global population:the changing epidemiology of disease and spinal disorders[J].Neurosurgery,2015,77(4):S1.
[2] 李秉新.全球老龄化趋势难逆转[N].人民日报,2017-06-30(022).
[3] YAMADA E.The fine structure of the gall bladder epithelium of the mouse[J].J Biophys Biochem Cytol,1955,1(5):445-458.
[4] CHENG J P X,NICHOLS B J.Caveolae:one function or many?[J].Trends Cell Biol,2016,26(3):177-189.
[5] SENGUPTA D.Cholesterol modulates the structure, binding modes, and energetics of Caveolin- membrane interactions[J].J Phys Chem B,2012,116(50):14556-14564.
[6] TRANE A E,HIOB M A,UY T,et al.Caveolin-1 scaffolding domain residue phenylalanine 92 modulates Akt signaling.[J].Eur J Pharmacol,2015(766):46-55.
[7] MAHMOOD J,ZAVERI S R,MURTI S C,et al.Caveolin-1:a novel prognostic biomarker of radioresistance in cancer[J].Int J Radiat Biol,2016,92(12):747-753.
[8] 葛亮,王桦,曾尔亢,等.衰老相关基因研究进展[J].中国老年学杂志,2014,34(22):6529-6532.
[9] 周璇,黄河浪,吴磊.端粒及其长度改变与人衰老关系的研究进展[J].中国老年学杂志,2015,35(5):1436-1438.
[10] 韩晶,杨泽.端粒—端粒酶与衰老退行性变的关系[J].中国老年保健医学,2015,13(5):21-24.
[11] 谢萨其拉古拉,孟柯.衰老机制及蒙医抗衰老研究进展[J].中国民族民间医药,2018,27(11):50-52.
[12] 夏世金,孙涛,吴俊珍.自由基、炎症与衰老[J].实用老年医学,2014(2):100-103.
[13] 张翠利,付丽娜,杨小云,等.活性氧自由基与细胞衰老关系的研究进展[J].广州化工,2015,43(19):5-7.
[14] 吴霞,隋明.细胞衰老与长寿[J].大家健康(学术版),2014,8(9):14-15.
[15] VOLONTE D,LIU Z,SHIVA S,et al.Caveolin-1 controls mitochondrial function through regulation of m-AAA mitochondrial protease[J].Aging,2016,8(10):2355-2369.
[16] 江莹,李顺,杨红,等.小窝蛋白-1与线粒体及癌症能量代谢—癌症治疗的新靶点[J].生物医学工程学杂志,2017,34(5):803-806.
[17] ODA T,SEKIMOTO T,KURASHIMA K,et al.Acute HSF1 depletion induces cellular senescence through the MDM2-p53-p21 pathway in human diploid fibroblasts.[J].J Cell Sci,2018,131(9):jcs.210724.
[18] VOLONTE D,VYAS A R,CHEN C,et al.Caveolin-1 promotes the tumor suppressor properties of oncogene-induced cellular senescence[J].J Biol Chem,2017,293(5):jbc.M117.815902.
[19] VOLONTE D,ZOU H,BARTHOLOMEW J N,et al.Oxidative stress-induced inhibition of Sirt1 by caveolin-1 promotes p53-dependent premature senescence and stimulates the secretion of interleukin 6(IL-6)[J].J Biol Chem,2015,290(7):4202-4214.
[20] AL-KHALAF H H,Aboussekhra A.p16 controls p53 protein expression through miR-dependent destabilization of MDM2[J].Molecular Cancer Research,2018.
[21] JIANG C,LIU G,LUCKHARDT T,et al.Serpine 1 induces alveolar type Ⅱ cell senescence through activating p53-p21-Rb pathway in fibrotic lung disease[J].Aging Cell,2017,16(5):1114-1124.
[22] LESSEL D,WU D,TRUJILLO C,et al.Dysfunction of the MDM2/p53 axis is linked to premature aging[J].J Clin Invest,2017,127(10):3598-3608.
[23] PARK W Y,PARK J S,CHO K A,et al.Up-regulation of caveolin attenuates epidermal growth factor signaling in senescent cells [J].J Biol Chem,2000,275(27):20847.
[24] CHO K A,RYU S J,PARK J S,et al.Senescent phenotype can be reversed by reduction of caveolin status[J].J Biol Chem,2003,278(30):27789-27795.
[25] CHEN P,YUAN Y,ZHANG T,et al.Pentosan polysulfate ameliorates apoptosis and inflammation by suppressing activation of the p38 MAPK pathway in high glucosetreated HK2 cells[J].Int J Mol Med,2018,41(2):908-914.
[26] CALLENDER L A,CARROLL E C,BEAL R,et al.Human CD8(+) EMRA T cells display a senescence-associated secretory phenotype regulated by p38 MAPK[J].Aging Cell,2017,17(1):1-9.
[27] SHIN S S,KO M C,PARK Y J,et al.Hydrangenol inhibits the proliferation,migration,and invasion of EJ bladder cancer cells via p21WAF1-mediated G1-phase cell cycle arrest,p38 MAPK activation,and reduction in Sp-1-induced MMP-9 expression[J].Excli J,2018(17):531-543.
[28] BRICHKINA A,NGUYEN N T,BASKAR R,et al.Proline isomerisation as a novel regulatory mechanism for p38MAPK activation and functions[J].Cell Death Differ,2016,23(10):1592-1601.
[29] MOMBACH J C,VENDRUSCULO B,BUGS C A.A Model for p38MAPK-Induced Astrocyte Senescence[J].PLoS One,2015,10(5):1-12.
[30] YU D M,JUNG S H,AN H T,et al.Caveolin-1 deficiency induces premature senescence with mitochondrial dysfunction[J].Aging Cell,2017,16(4):773-784.
[31] DASARI A, BARTHOLOMEW J N, VOLONTE D, et al.Oxidative stress induces premature senescence by stimulating Caveolin-1 gene transcription through p38 mitogen-activated protein kinase/Sp1-mediated activation of two GC-Rich promoter elements[J].Cancer Res,2006,66(22):10805-10814.
[32] HUI W,YOUNG D A,ROWAN A D,et al.Oxidative changes and signalling pathways are pivotal in initiating age-related changes in articular cartilage[J].Ann Rheum Dis,2014,75(2):449.
[33] LI Z Y,CHEN Z L,ZHANG T,et al.TGF-β and NF-κB signaling pathway crosstalk potentiates corneal epithelial senescence through an RNA stress response[J].Aging,2016,8(10):2337-2350.
[34] ANNAMARIA L,VANESSA P,ARIANNA B,et al.NF-κB in innate neuroprotection and age-related neurodegenerative diseases[J].Front Neurol,2015,6(98):98.
[35] MA X,DANG C,KANG H,et al.Saikosaponin-D reduces cisplatin-induced nephrotoxicity by repressing ROS-mediated activation of MAPK and NF-κB signalling pathways[J].Int Immunopharmacol,2015,28(1):399-408.
[36] TIRUPPATHI C,SHIMIZU J,MIYAWAKI-SHIMIZU K,et al.Role of NF-κB-dependent caveolin-1 expression in the mechanism of increased endothelial permeability induced by lipopolysaccharide[J].J Biol Chem,2008,283(7):4210.
[2] 李秉新.全球老龄化趋势难逆转[N].人民日报,2017-06-30(022).
[3] YAMADA E.The fine structure of the gall bladder epithelium of the mouse[J].J Biophys Biochem Cytol,1955,1(5):445-458.
[4] CHENG J P X,NICHOLS B J.Caveolae:one function or many?[J].Trends Cell Biol,2016,26(3):177-189.
[5] SENGUPTA D.Cholesterol modulates the structure, binding modes, and energetics of Caveolin- membrane interactions[J].J Phys Chem B,2012,116(50):14556-14564.
[6] TRANE A E,HIOB M A,UY T,et al.Caveolin-1 scaffolding domain residue phenylalanine 92 modulates Akt signaling.[J].Eur J Pharmacol,2015(766):46-55.
[7] MAHMOOD J,ZAVERI S R,MURTI S C,et al.Caveolin-1:a novel prognostic biomarker of radioresistance in cancer[J].Int J Radiat Biol,2016,92(12):747-753.
[8] 葛亮,王桦,曾尔亢,等.衰老相关基因研究进展[J].中国老年学杂志,2014,34(22):6529-6532.
[9] 周璇,黄河浪,吴磊.端粒及其长度改变与人衰老关系的研究进展[J].中国老年学杂志,2015,35(5):1436-1438.
[10] 韩晶,杨泽.端粒—端粒酶与衰老退行性变的关系[J].中国老年保健医学,2015,13(5):21-24.
[11] 谢萨其拉古拉,孟柯.衰老机制及蒙医抗衰老研究进展[J].中国民族民间医药,2018,27(11):50-52.
[12] 夏世金,孙涛,吴俊珍.自由基、炎症与衰老[J].实用老年医学,2014(2):100-103.
[13] 张翠利,付丽娜,杨小云,等.活性氧自由基与细胞衰老关系的研究进展[J].广州化工,2015,43(19):5-7.
[14] 吴霞,隋明.细胞衰老与长寿[J].大家健康(学术版),2014,8(9):14-15.
[15] VOLONTE D,LIU Z,SHIVA S,et al.Caveolin-1 controls mitochondrial function through regulation of m-AAA mitochondrial protease[J].Aging,2016,8(10):2355-2369.
[16] 江莹,李顺,杨红,等.小窝蛋白-1与线粒体及癌症能量代谢—癌症治疗的新靶点[J].生物医学工程学杂志,2017,34(5):803-806.
[17] ODA T,SEKIMOTO T,KURASHIMA K,et al.Acute HSF1 depletion induces cellular senescence through the MDM2-p53-p21 pathway in human diploid fibroblasts.[J].J Cell Sci,2018,131(9):jcs.210724.
[18] VOLONTE D,VYAS A R,CHEN C,et al.Caveolin-1 promotes the tumor suppressor properties of oncogene-induced cellular senescence[J].J Biol Chem,2017,293(5):jbc.M117.815902.
[19] VOLONTE D,ZOU H,BARTHOLOMEW J N,et al.Oxidative stress-induced inhibition of Sirt1 by caveolin-1 promotes p53-dependent premature senescence and stimulates the secretion of interleukin 6(IL-6)[J].J Biol Chem,2015,290(7):4202-4214.
[20] AL-KHALAF H H,Aboussekhra A.p16 controls p53 protein expression through miR-dependent destabilization of MDM2[J].Molecular Cancer Research,2018.
[21] JIANG C,LIU G,LUCKHARDT T,et al.Serpine 1 induces alveolar type Ⅱ cell senescence through activating p53-p21-Rb pathway in fibrotic lung disease[J].Aging Cell,2017,16(5):1114-1124.
[22] LESSEL D,WU D,TRUJILLO C,et al.Dysfunction of the MDM2/p53 axis is linked to premature aging[J].J Clin Invest,2017,127(10):3598-3608.
[23] PARK W Y,PARK J S,CHO K A,et al.Up-regulation of caveolin attenuates epidermal growth factor signaling in senescent cells [J].J Biol Chem,2000,275(27):20847.
[24] CHO K A,RYU S J,PARK J S,et al.Senescent phenotype can be reversed by reduction of caveolin status[J].J Biol Chem,2003,278(30):27789-27795.
[25] CHEN P,YUAN Y,ZHANG T,et al.Pentosan polysulfate ameliorates apoptosis and inflammation by suppressing activation of the p38 MAPK pathway in high glucosetreated HK2 cells[J].Int J Mol Med,2018,41(2):908-914.
[26] CALLENDER L A,CARROLL E C,BEAL R,et al.Human CD8(+) EMRA T cells display a senescence-associated secretory phenotype regulated by p38 MAPK[J].Aging Cell,2017,17(1):1-9.
[27] SHIN S S,KO M C,PARK Y J,et al.Hydrangenol inhibits the proliferation,migration,and invasion of EJ bladder cancer cells via p21WAF1-mediated G1-phase cell cycle arrest,p38 MAPK activation,and reduction in Sp-1-induced MMP-9 expression[J].Excli J,2018(17):531-543.
[28] BRICHKINA A,NGUYEN N T,BASKAR R,et al.Proline isomerisation as a novel regulatory mechanism for p38MAPK activation and functions[J].Cell Death Differ,2016,23(10):1592-1601.
[29] MOMBACH J C,VENDRUSCULO B,BUGS C A.A Model for p38MAPK-Induced Astrocyte Senescence[J].PLoS One,2015,10(5):1-12.
[30] YU D M,JUNG S H,AN H T,et al.Caveolin-1 deficiency induces premature senescence with mitochondrial dysfunction[J].Aging Cell,2017,16(4):773-784.
[31] DASARI A, BARTHOLOMEW J N, VOLONTE D, et al.Oxidative stress induces premature senescence by stimulating Caveolin-1 gene transcription through p38 mitogen-activated protein kinase/Sp1-mediated activation of two GC-Rich promoter elements[J].Cancer Res,2006,66(22):10805-10814.
[32] HUI W,YOUNG D A,ROWAN A D,et al.Oxidative changes and signalling pathways are pivotal in initiating age-related changes in articular cartilage[J].Ann Rheum Dis,2014,75(2):449.
[33] LI Z Y,CHEN Z L,ZHANG T,et al.TGF-β and NF-κB signaling pathway crosstalk potentiates corneal epithelial senescence through an RNA stress response[J].Aging,2016,8(10):2337-2350.
[34] ANNAMARIA L,VANESSA P,ARIANNA B,et al.NF-κB in innate neuroprotection and age-related neurodegenerative diseases[J].Front Neurol,2015,6(98):98.
[35] MA X,DANG C,KANG H,et al.Saikosaponin-D reduces cisplatin-induced nephrotoxicity by repressing ROS-mediated activation of MAPK and NF-κB signalling pathways[J].Int Immunopharmacol,2015,28(1):399-408.
[36] TIRUPPATHI C,SHIMIZU J,MIYAWAKI-SHIMIZU K,et al.Role of NF-κB-dependent caveolin-1 expression in the mechanism of increased endothelial permeability induced by lipopolysaccharide[J].J Biol Chem,2008,283(7):4210.