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Effects of exercise preconditioning on NLRP3 and mitochondrial fission in isoproterenol-induced myocardial infarcted rats

Effects of exercise preconditioning on NLRP3 and mitochondrial fission in isoproterenol-induced... Myocardial infarction is a common disease that causes morbidity and mortality in human. Exercise training is an effective strategy to improve cardioprotection. The signaling pathways of exercise preconditioning on the reduction of MI-induced cardiac injuries is one of the topics that has attracted a lot of attention. The purpose of this study was to investigate the effects of exercise preconditioning on cardiac damage and dynamin-related protein 1 (Drp1) as an effective factor for activating the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) following myocardial infarction (MI). Twenty male Wistar rats were randomly divided into 4 groups of high-intensity interval training + myocardial infarction (HIIT + MI), control + myocardial infarction (CON + MI), HIIT, and sham. Training groups performed 4 weeks (5 days per week) of HIIT. The training protocol consisted of 10*1-min running intervals were separated by a 2-min rest. The training intensity varied every week. For induction of MI, an injection of isoproterenol was used. Creatine kinase-myoglobin binding (CK-MB), lactate dehydrogenase (LDH), Drp1, and NLRP3 gene expression were measured. The results of the present study showed that CK-MB and LDH in CON + MI group were significantly higher than in the HIIT + MI group (P ˂ 0.05). Myocardial infarction results in a significant increase in Drp1 gene expression in the CON + MI and HIIT + MI groups relative to the sham group. The expression of the Drp1 gene was lower in the HIIT + MI group than in the CON + MI group, but it was insignificant. Moreover, NLRP3 in the CON + MI group had a remarkable increase compared with HIIT + MI, HIIT, and sham groups (P ˃ 0.05). Four weeks of exercise preconditioning reduced injury and necrosis in cardiac tissue and can increase cardioprotection. Although NLRP3 inflammasome was reduced due to exercise training, it had no significant decrease in Drp1 expression which may indicate the need for a longer training period. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Comparative Clinical Pathology Springer Journals

Effects of exercise preconditioning on NLRP3 and mitochondrial fission in isoproterenol-induced myocardial infarcted rats

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Springer Journals
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Copyright © The Author(s), under exclusive licence to Springer-Verlag London Ltd., part of Springer Nature 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
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10.1007/s00580-022-03397-3
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Abstract

Myocardial infarction is a common disease that causes morbidity and mortality in human. Exercise training is an effective strategy to improve cardioprotection. The signaling pathways of exercise preconditioning on the reduction of MI-induced cardiac injuries is one of the topics that has attracted a lot of attention. The purpose of this study was to investigate the effects of exercise preconditioning on cardiac damage and dynamin-related protein 1 (Drp1) as an effective factor for activating the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) following myocardial infarction (MI). Twenty male Wistar rats were randomly divided into 4 groups of high-intensity interval training + myocardial infarction (HIIT + MI), control + myocardial infarction (CON + MI), HIIT, and sham. Training groups performed 4 weeks (5 days per week) of HIIT. The training protocol consisted of 10*1-min running intervals were separated by a 2-min rest. The training intensity varied every week. For induction of MI, an injection of isoproterenol was used. Creatine kinase-myoglobin binding (CK-MB), lactate dehydrogenase (LDH), Drp1, and NLRP3 gene expression were measured. The results of the present study showed that CK-MB and LDH in CON + MI group were significantly higher than in the HIIT + MI group (P ˂ 0.05). Myocardial infarction results in a significant increase in Drp1 gene expression in the CON + MI and HIIT + MI groups relative to the sham group. The expression of the Drp1 gene was lower in the HIIT + MI group than in the CON + MI group, but it was insignificant. Moreover, NLRP3 in the CON + MI group had a remarkable increase compared with HIIT + MI, HIIT, and sham groups (P ˃ 0.05). Four weeks of exercise preconditioning reduced injury and necrosis in cardiac tissue and can increase cardioprotection. Although NLRP3 inflammasome was reduced due to exercise training, it had no significant decrease in Drp1 expression which may indicate the need for a longer training period.

Journal

Comparative Clinical Pathology – Springer Journals

Published: Sep 23, 2022

Keywords: Cardiac tissue; Exercise preconditioning; Mitochondrial fission; HIIT; Inflammasome

References

  • Regulatory mechanisms of the NLRP3 inflammasome, a novel immune-inflammatory marker in cardiovascular diseases
    An, N; Gao, Y; Si, Z; Zhang, H; Wang, L
  • Mitochondrial dynamics—mitochondrial fission and fusion in human diseases
    Archer, SL
  • Mechanisms involved in exercise-induced cardioprotection: a systematic review
    Borges, JP; Lessa, MA
  • Inhibition of mitochondrial fission as a novel therapeutic strategy to reduce mortality upon myocardial infarction
    Cooper, HA; Eguchi, S
  • Acute inhibition of excessive mitochondrial fission after myocardial infarction prevents long-term cardiac dysfunction
    Disatnik, MH; Ferreira, JC; Campos, JC; Gomes, KS; Dourado, PM
  • Exercise-induced cardiac preconditioning: how exercise protects your achy-breaky heart
    Frasier, CR; Moore, RL; Brown, DA
  • ER tubules mark sites of mitochondrial division
    Friedman, JR; Lackner, LL; West, M; DiBenedetto, JR; Nunnari, J
  • Mitochondrial dynamics as an underlying mechanism involved in aerobic exercise training-induced cardioprotection against ischemia-reperfusion injury
    Ghahremani, R; Damirchi, A; Salehi, I; Komaki, A; Esposito, F
  • The effect of preconditioning with high-intensity training on tissue levels of G-CSF, its receptor and C-kit after an acute myocardial infarction in male rats
    Ghanimati, R; Rajabi, H; Ramezani, F; Ramez, M; Bapiran, M
  • Running speed and maximal oxygen uptake in rats and mice: practical implications for exercise training
    Høydal, MA; Wisløff, U; Kemi, OJ; Ellingsen, Ø
  • Aerobic interval training attenuates mitochondrial dysfunction in rats post-myocardial infarction: roles of mitochondrial network dynamics
    Jiang, H-K; Wang, Y-H; Sun, L; He, X; Zhao, M
  • Exercise induces a cardiac mitochondrial phenotype that resists apoptotic stimuli
    Kavazis, AN; McClung, JM; Hood, DA; Powers, SK
  • Inflammasome activation of cardiac fibroblasts is essential for myocardial ischemia/reperfusion injury
    Kawaguchi, M; Takahashi, M; Hata, T; Kashima, Y; Usui, F
  • The NLRP3 inflammasome: an overview of mechanisms of activation and regulation
    Kelley, N; Jeltema, D; Duan, Y; He, Y
  • Combined effects of resistance training and calorie restriction on mitochondrial fusion and fission proteins in rat skeletal muscle
    Kitaoka, Y; Nakazato, K; Ogasawara, R
  • Physical activity protects NLRP 3 inflammasome‐associated coronary vascular dysfunction in obese mice
    Lee, J; Lee, Y; LaVoy, EC; Umetani, M; Hong, J
  • The molecular links between cell death and inflammasome
    Lee, K-H; Kang, T-B
  • Strenuous exercise induces mitochondrial damage in skeletal muscle of old mice
    Lee, S; Kim, M; Lim, W; Kim, T; Kang, C
  • TXNIP mediates NLRP3 inflammasome activation in cardiac microvascular endothelial cells as a novel mechanism in myocardial ischemia/reperfusion injury
    Liu, Y; Lian, K; Zhang, L; Wang, R; Yi, F
  • Absence of NLRP3 inflammasome in hematopoietic cells reduces adverse remodeling after experimental myocardial infarction
    Louwe, MC; Olsen, MB; Kaasbøll, OJ; Yang, K; Fosshaug, LE
  • Roles of mitochondrial dynamics modulators in cardiac ischaemia/reperfusion injury
    Maneechote, C; Palee, S; Chattipakorn, SC; Chattipakorn, N
  • NLRP3 inflammasome in acute myocardial infarction
    Mauro, AG; Bonaventura, A; Mezzaroma, E; Quader, M; Toldo, S
  • Impact of resistance training on the autophagy-inflammation-apoptosis crosstalk in elderly subjects
    Mejías-Peña, Y; Estébanez, B; Rodriguez-Miguelez, R; Fernandez-Gonzalo, R; Almar, M
  • The inflammasome promotes adverse cardiac remodeling following acute myocardial infarction in the mouse
    Mezzaroma, E; Toldo, S; Farkas, D; Seropian, IM; Van Tassell, BW
  • Mitochondrial dysfunction as a driver of NLRP3 inflammasome activation and its modulation through mitophagy for potential therapeutics
    Mishra, SR; Mahapatra, KK; Behera, BP; Patra, S; Bhol, CS
  • Inhibiting mitochondrial fission protects the heart against ischemia/reperfusion injury
    Ong, S-B; Subrayan, S; Lim, SY; Yellon, DM; Davidson, SM
  • Defective mitochondrial fission augments NLRP3 inflammasome activation
    Park, S; Won, J-H; Hwang, I; Hong, S; Lee, HK
  • Mechanisms involved in cardioprotection induced by physical exercise
    Penna, C; Alloatti, G; Crisafulli, A
  • Mechanisms of exercise-induced cardioprotection
    Powers, SK; Smuder, AJ; Kavazis, AN; Quindry, JC
  • Exercise preconditioning as a cardioprotective phenotype
    Quindry, JC; Franklin, BA
  • Ischemia reperfusion injury, KATP channels, and exercise-induced cardioprotection against apoptosis
    Quindry, JC; Miller, L; McGinnis, G; Kliszczewicz, B; Irwin, JM
  • The effect of high-intensity interval training on cardioprotection against ischemia-reperfusion injury in Wistar rats
    Rahimi, M; Shekarforoush, S; Asgari, AR; Khoshbaten, A; Rajabi, H
  • Mitochondria in acute myocardial infarction and cardioprotection
    Ramachandra, CJ; Hernandez-Resendiz, S; Crespo-Avilan, GE; Lin, Y-H; Hausenloy, DJ
  • Inhibitors of mitochondrial fission as a therapeutic strategy for diseases with oxidative stress and mitochondrial dysfunction
    Reddy, PH
  • Acute myocardial infarction
    Reed, GW; Rossi, JE; Cannon, CP
  • Mitochondria, the NLRP3 inflammasome, and sirtuins in type 2 diabetes: new therapeutic targets
    Rovira-Llopis, S; Apostolova, N; Banuls, C; Muntane, J; Rocha, M
  • The NLRP3 inflammasome is up-regulated in cardiac fibroblasts and mediates myocardial ischaemia–reperfusion injury
    Sandanger, Ø; Ranheim, T; Vinge, LE; Bliksøen, M; Alfsnes, K
  • Inhibition of the mitochondrial fission protein Drp1 improves survival in a murine cardiac arrest model
    Sharp, WW; Beiser, DG; Fang, YH; Han, M; Piao, L
  • β-Adrenoreceptor agonist isoproterenol alters oxidative status, inflammatory signaling, injury markers and apoptotic cell death in myocardium of rats
    Shukla, SK; Sharma, SB
  • Mitochondria and cell signalling
    Tait, SW; Green, DR
  • NLRP3 inflammasome as a novel player in myocardial infarction
    Takahashi, M
  • Mitochondrial dynamics in exercise physiology
    Tanaka, T; Nishimura, A; Nishiyama, K; Goto, T; Numaga-Tomita, T
  • Association of exercise preconditioning with immediate cardioprotection: a review
    Thijssen, DH; Redington, A; George, KP; Hopman, MT; Jones, H
  • Exercise and mitochondrial dynamics: keeping in shape with ROS and AMPK
    Trewin, AJ; Berry, BJ; Wojtovich, AP
  • Effect of high-intensity interval training on cardiac structure and function in rats with acute myocardial infarct
    Wang, B; Zhou, R; Wang, Y; Liu, X; Shou, X
  • Targeting NLRP3 (nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3) inflammasome in cardiovascular disorders
    Wang, Z; Hu, W; Lu, C; Ma, Z; Jiang, S
  • Long-term aerobic exercise protects the heart against ischemia/reperfusion injury via PI3 kinase-dependent and Akt-mediated mechanism
    Zhang, K-R; Liu, H-T; Zhang, H-F; Zhang, Q-J; Li, Q-X
  • Exercise training in hypoxia prevent hypoxia induced NLRP3 inflammasome activation in skeletal muscles
    Zhang, Z; Hai, B; Yang, S; Wang, T; Yuan, Y
  • A role for mitochondria in NLRP3 inflammasome activation
    Zhou, R; Yazdi, AS; Menu, P; Tschopp, J
  • PEDF inhibits the activation of NLRP3 inflammasome in hypoxia cardiomyocytes through PEDF receptor/phospholipase A2
    Zhou, Z; Wang, Z; Guan, Q; Qiu, F; Li, Y