Dynamic resistance exercise increases skeletal muscle-derived FSTL1 inducing cardiac angiogenesis via DIP2A-Smad2/3 in rats following myocardial infarction  被引量:18

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作  者:Yue Xi Meili Hao Qiaoqin Liang Yongxia Li Da-Wei Gong Zhenjun Tian 

机构地区:[1]Institute of Sports and Exercise Biology,Shaanxi Normal University,Xi’an 710119,China [2]School of Physical Education,Luoyang Normal University,Luoyang 471934,China [3]School of Life Science,Shaanxi Normal University,Xi’an 710119,China [4]Division of Endocrinology,Diabetes and Nutrition,Department of Medicine,University of Maryland School of Medicine,Baltimore,MD 21201,USA

出  处:《Journal of Sport and Health Science》2021年第5期594-603,共10页运动与健康科学(英文)

基  金:supported this research:The National Natural Science Foundation of China(No.31671240 to ZT,No.31900828 to YX).

摘  要:Purpose:The aim of this study was to investigate the potential of dynamic resistance exercise to generate skeletal muscle-derived follistatin like-1(FSTL1),which may induce cardioprotection in rats following myocardial infarction(MI)by inducing angiogenesis.Methods:Male,adult Sprague-Dawley rats were randomly divided into 5 groups(n=12 in each group):sham group(S),sedentary MI group(MI),MI+resistance exercise group(MR),MI+adeno-associated virus(AAV)-FSTL1 injection group(MA),and MI+AAV-FSTL1 injection+resistance exercise group(MAR).The AAV-FSTL1 vector was prepared by molecular biology methods and injected into the anterior tibialis muscle.The MI model was established by ligation of the left anterior descending coronary artery.Rats in the MR and MAR groups underwent 4 weeks of dynamic resistance exercise training using a weighted climbing-up ladder.Heart function was evaluated by hemodynamic measures.Collagen volume fraction of myocardium was observed and analyzed by Masson’s staining.Human umbilical vein vessel endothelial cells culture and recombinant human FSTL1 protein or transforming growth factor-b receptor 1(TGFbR1)inhibitor treatment were used to elucidate the molecular signaling mechanism of FSTL1.Angiogenesis,cell proliferation,and disco interacting protein 2 homolog A(DIP2A)location were observed by immunofluorescence staining.The expression of FSTL1,DIP2A,and the activation of signaling pathways were detected by Western blotting.Angiogenesis of endothelial cells was observed by tubule experiment.One-way analysis of variance and Student’s t test were used for statistical analysis.Results:Resistance exercise stimulated the secretion of skeletal muscle FSTL1,which promoted myocardial angiogenesis,inhibited pathological remodeling,and protected cardiac function in MI rats.Exercise facilitated skeletal muscle FSTL1 to play a role in protecting the heart.Exogenous FSTL1 promoted the human umbilical vein vessel endothelial cells proliferation and up-regulated the expression of DIP2A,while TGFbR1 inhibito

关 键 词:ANGIOGENESIS Follistatin like-1 Myocardial infarction Resistance exercise Signaling mechanism 

分 类 号:R87[医药卫生—运动医学]

 

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