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典型文献
Exercise attenuates angiotensinⅡ-induced muscle atrophy by targeting PPARγ/miR-29b
文献摘要:
Background:Exercise is beneficial for muscle atrophy.Peroxisome proliferator-activated receptor gamma(PPARγ)and microRNA-29b(miR-29b)have been reported to be responsible for angiotensinⅡ(AngⅡ)-induced muscle atrophy.However,it is unclear whether exercise can protect AngⅡ-induced muscle atrophy by targeting PPARγ/miR-29b.Methods:Skeletal muscle atrophy in both the control group and the run group was established by AngⅡ infusion;after 1 week of exercise train-ing,the mice were sacrificed,and muscle weight was determined.Myofiber size was measured by hematoxylin-eosin and wheat-germ agglutinin staining.Apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling staining.The expression level of muscle atrogenes,including F-box only protein 32(FBXO32,also called Atrogin-1)and muscle-specific RING-finger 1(MuRF-1),the phosphorylation level of protein kinase B(PKB,also called AKT)/forkhead box O3A(FOXO3A)/mammalian target of rapamycin(mTOR)pathway proteins,the expression level of PPARγ and apoptosis-related proteins,including B-cell lymphoma-2(Bcl-2),Bcl-2-associated X(Bax),cysteine-aspartic acid protease 3(caspase-3),and cleaved-caspase-3,were determined by western blot.The expression level of miR-29b was checked by reverse-transcription quantitative polymerase chain reaction.A PPARγ inhibitor(T0070907)or adeno-associated virus serotype-8(AAV8)-mediated miR-29b overexpression was used to demonstrate whether PPARγ activation or miR-29b inhibition mediates the beneficial effects of exercise in AngⅡ-induced muscle atrophy.Results:Exercise can significantly attenuate AngⅡ-induced muscle atrophy,which is demonstrated by increased skeletal muscle weight,cross-sectional area of myofiber,and activation of AKT/mTOR signaling and by decreased atrogenes expressions and apoptosis.In AngⅡ-induced muscle atrophy mice models,PPAR-γ was elevated whereas miR-29b was decreased by exercise.The protective effects of exercise in AngⅡ-induced muscle atrophy were inhibited by a PPARγ inhibitor(T0070907)or adeno-associated virus serotype-8(AAV8)-mediated miR-29b overexpression.Conclusion:Exercise attenuates AngⅡ-induced muscle atrophy by activation of PPARγ and suppression of miR-29b.
文献关键词:
作者姓名:
Qi Liua;Liyang Chena;Xuchun Liang;Yuqing Cao;Xinyue Zhu;Siqi Wang;Jin Li;Juan Gao;Junjie Xiao
作者机构:
Cardiac Regeneration and Ageing Lab,Institute of Cardiovascular Sciences,School of Life Science,Shanghai University,Shanghai 200444,China;Shanghai Engineering Research Center of Organ Repair,School of Medicine,Shanghai University,Shanghai 200444,China
引用格式:
[1]Qi Liua;Liyang Chena;Xuchun Liang;Yuqing Cao;Xinyue Zhu;Siqi Wang;Jin Li;Juan Gao;Junjie Xiao-.Exercise attenuates angiotensinⅡ-induced muscle atrophy by targeting PPARγ/miR-29b)[J].运动与健康科学(英文),2022(06):696-707
A类:
Myofiber,atrogenes,T0070907,myofiber
B类:
Exercise,attenuates,angiotensin,induced,muscle,atrophy,by,targeting,PPAR,miR,29b,Background,beneficial,Peroxisome,proliferator,activated,receptor,gamma,microRNA,have,been,reported,responsible,Ang,However,unclear,whether,exercise,Methods,Skeletal,both,control,group,run,was,established,infusion,after,week,train,mice,were,sacrificed,weight,determined,size,measured,hematoxylin,eosin,wheat,germ,agglutinin,staining,Apoptosis,evaluated,terminal,deoxynucleotidyl,transferase,dUTP,nick,end,labeling,level,including,box,only,FBXO32,also,called,Atrogin,specific,RING,finger,MuRF,phosphorylation,kinase,PKB,AKT,forkhead,FOXO3A,mammalian,rapamycin,mTOR,pathway,proteins,apoptosis,related,cell,lymphoma,Bcl,associated,Bax,cysteine,aspartic,acid,protease,caspase,cleaved,western,blot,checked,reverse,transcription,quantitative,polymerase,chain,reaction,inhibitor,adeno,virus,serotype,AAV8,mediated,overexpression,used,activation,inhibition,mediates,effects,Results,significantly,which,demonstrated,increased,skeletal,cross,sectional,area,signaling,decreased,expressions,In,models,elevated,whereas,protective,inhibited,Conclusion,suppression
AB值:
0.468298
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