HSF1 and NF-κB p65 participate in the process of exercise preconditioning attenuating pressure overload-induced pathological cardiac hypertrophy

Xu, Tongyi; Zhang, Ben; Yang, Fan; Cai, Chengliang; Wang, Guokun; Han, Qingqi; Zou, Liangjian

doi:10.1016/J.BBRC.2015.03.079

Title: HSF1 and NF-κB p65 participate in the process of exercise preconditioning attenuating pressure overload-induced pathological cardiac hypertrophy

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Abstract

Pathological cardiac hypertrophy, often accompanied by hypertension, aortic stenosis and valvular defects, is typically associated with myocyte remodeling and cardiac dysfunction. Exercise preconditioning (EP) has been proven to enhance the tolerance of the myocardium to cardiac ischemia-reperfusion injury. However, the effects of EP in pathological cardiac hypertrophy are rarely reported. 10-wk-old male Sprague–Dawley rats (n = 80) were randomly divided into four groups: sham, TAC, EP + sham and EP + TAC. Two EP groups were subjected to 4 weeks of treadmill training, and the EP + TAC and TAC groups were followed by TAC operations. The sham and EP + sham groups underwent the same operation without aortic constriction. Eight weeks after the surgery, we evaluated the effects of EP by echocardiography, morphology, and histology and observed the expressions of the associated proteins. Compared with the respective control groups, hypertrophy-related indicators were significantly increased in the TAC and EP + TAC groups (p < 0.05). However, between the TAC and EP + TAC groups, all of these changes were effectively inhibited by EP treatment (p < 0.05). Furthermore, EP treatment upregulated the expression of HSF1 and HSP70, increased the HSF1 levels in the nuclear fraction, inhibited the expression of the NF-κB p65 subunit, decreased the NF-κB p65 subunit levels in the nuclear fraction, and reduced the IL2more »« less

Authors:

Xu, Tongyi ^[1]; Zhang, Ben ^[2]; Yang, Fan; Cai, Chengliang; Wang, Guokun ^[3]; Han, Qingqi ^[3]; Zou, Liangjian ^[3]

Department of Cardiothoracic Surgery, No. 401 Hospital of PLA, Qingdao (China)
Centre of Cardiovascular Surgery, Guangzhou General Hospital of Guangzhou Military Region, Guangzhou (China)
Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai (China)

Publication Date:: Fri May 08 00:00:00 EDT 2015

OSTI Identifier:: 22458543

Resource Type:: Journal Article

Journal Name:: Biochemical and Biophysical Research Communications

Additional Journal Information:: Journal Volume: 460; Journal Issue: 3; Other Information: Copyright (c) 2015 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X

Country of Publication:: United States

Language:: English

Subject:: 60 APPLIED LIFE SCIENCES; BRAIN; COMPARATIVE EVALUATIONS; EXERCISE; HEAT-SHOCK PROTEINS; HISTOLOGY; HYPERTENSION; HYPERTROPHY; INDICATORS; INJURIES; ISCHEMIA; MORPHOLOGY; MYOCARDIUM; PEPTIDES; RATS; SURGERY; TRAINING; TRANSCRIPTION FACTORS

Citation Formats


                    Xu, Tongyi, Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, Zhang, Ben, Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, Yang, Fan, Cai, Chengliang, Wang, Guokun, Han, Qingqi, and Zou, Liangjian. HSF1 and NF-κB p65 participate in the process of exercise preconditioning attenuating pressure overload-induced pathological cardiac hypertrophy.  United States: N. p., 2015. 
        Web.  doi:10.1016/J.BBRC.2015.03.079.

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                    Xu, Tongyi, Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, Zhang, Ben, Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, Yang, Fan, Cai, Chengliang, Wang, Guokun, Han, Qingqi, & Zou, Liangjian. HSF1 and NF-κB p65 participate in the process of exercise preconditioning attenuating pressure overload-induced pathological cardiac hypertrophy.  United States.  https://doi.org/10.1016/J.BBRC.2015.03.079

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                    Xu, Tongyi, Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, Zhang, Ben, Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, Yang, Fan, Cai, Chengliang, Wang, Guokun, Han, Qingqi, and Zou, Liangjian. 2015.  
        "HSF1 and NF-κB p65 participate in the process of exercise preconditioning attenuating pressure overload-induced pathological cardiac hypertrophy".  United States.  https://doi.org/10.1016/J.BBRC.2015.03.079.

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@article{osti_22458543,

  title        = {HSF1 and NF-κB p65 participate in the process of exercise preconditioning attenuating pressure overload-induced pathological cardiac hypertrophy},

  author       = {Xu, Tongyi and Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai and Zhang, Ben and Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai and Yang, Fan and Cai, Chengliang and Wang, Guokun and Han, Qingqi and Zou, Liangjian},

  abstractNote = {Pathological cardiac hypertrophy, often accompanied by hypertension, aortic stenosis and valvular defects, is typically associated with myocyte remodeling and cardiac dysfunction. Exercise preconditioning (EP) has been proven to enhance the tolerance of the myocardium to cardiac ischemia-reperfusion injury. However, the effects of EP in pathological cardiac hypertrophy are rarely reported. 10-wk-old male Sprague–Dawley rats (n = 80) were randomly divided into four groups: sham, TAC, EP + sham and EP + TAC. Two EP groups were subjected to 4 weeks of treadmill training, and the EP + TAC and TAC groups were followed by TAC operations. The sham and EP + sham groups underwent the same operation without aortic constriction. Eight weeks after the surgery, we evaluated the effects of EP by echocardiography, morphology, and histology and observed the expressions of the associated proteins. Compared with the respective control groups, hypertrophy-related indicators were significantly increased in the TAC and EP + TAC groups (p < 0.05). However, between the TAC and EP + TAC groups, all of these changes were effectively inhibited by EP treatment (p < 0.05). Furthermore, EP treatment upregulated the expression of HSF1 and HSP70, increased the HSF1 levels in the nuclear fraction, inhibited the expression of the NF-κB p65 subunit, decreased the NF-κB p65 subunit levels in the nuclear fraction, and reduced the IL2 levels in the myocardia of rats. EP could effectively reduce the cardiac hypertrophic responses induced by TAC and may play a protective role by upregulating the expressions of HSF1 and HSP70, activating HSF1 and then inhibiting the expression of NF-κB p65 and nuclear translocation. - Highlights: • EP could effectively reduce the cardiac hypertrophic responses induced by TAC. • EP may play a protective role by upregulating the expressions of HSF1 and HSP70 and then activating HSF1. • EP may play a protective role by inhibiting the expression of NF-κB p65 and nuclear translocation.},

  doi          = {10.1016/J.BBRC.2015.03.079},

  url          = {https://www.osti.gov/biblio/22458543},
  journal      = {Biochemical and Biophysical Research Communications},

  issn         = {0006-291X},

  number       = 3,

  volume       = 460,

  place        = {United States},

  year         = {Fri May 08 00:00:00 EDT 2015},

  month        = {Fri May 08 00:00:00 EDT 2015}

}

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