Top

Published in:

01-06-2022 | Myocardial Infarction

PM_2.5 Exposure Lowers Mitochondrial Endurance During Cardiac Recovery in a Rat Model of Myocardial Infarction

Authors: Bhavana Sivakumar, Gino A. Kurian

Published in: Cardiovascular Toxicology | Issue 6/2022

Abstract

Many studies have reported the negative effect of PM_2.5 exposure on heart function which is likely to impair postcardiac surgery rehabilitation that is involved in recovery and wound healing, yet the direct effects of PM_2.5 from diesel exhaust (DPM) on cardiac recovery is unknown. To study the impact of DPM on cardiac recovery and repair, we utilized isoproterenol induced myocardial infarction (MI) model where female rats were exposed to DPM prior and after MI induction. The experimental groups comprise of normal, ISO control, DPM control (42 days of exposure), DPM exposed prior (21 days) and after (21 days) MI induction (D + I + D) and DPM exposed (21 days) after MI (I + D). Post-MI rat hearts from D + I + D group exhibited higher fibrosis, elevated cardiac injury and altered electrophysiology, where this pathology was also observed in I + D group animals which was mild. Loss of mitochondrial quality was evident in DPM exposed animals with and without MI, where severe mitochondrial damage persisted in D + I + D group. In addition, these animals showed striking decline in ETC enzyme activity, ATP levels, mitochondrial copy number and down regulation of PGC1-α, TFAM and POLG along with the genes involved in mitophagy and mitofusion. Besides, the MI associated inactivation of cardio protective signalling pathways like PI3K and Akt were persistent in D + I + D group. In fact, I + D group animals also showed a similar pattern of change, but in a mild form. Taken together, exposure to PM_2.5 increases the risk, frequency or progression of MI by impairing the recovery potential of the myocardium.

Bhatt, A. S., Ambrosy, A. P., & Velazquez, E. J. (2017). Adverse remodeling and reverse remodeling after myocardial infarction. Current Cardiology Reports, 19(8), 71. https://doi.org/10.1007/s11886-017-0876-4CrossRefPubMed

Sutton, M. G., & Sharpe, N. (2000). Left ventricular remodeling after myocardial infarction: Pathophysiology and therapy. Circulation, 101(25), 2981–2988. https://doi.org/10.1161/01.cir.101.25.2981CrossRefPubMed

French, B. A., & Kramer, C. M. (2007). Mechanisms of post-infarct left ventricular remodeling. Drug Discovery Today: Disease Mechanisms, 4(3), 185–196. https://doi.org/10.1016/j.ddmec.2007.12.006CrossRefPubMed

Woo, K. S., & White, H. D. (1994). Factors affecting outcome after recovery from myocardial infarction. Annual Review of Medicine, 45, 325–339. https://doi.org/10.1146/annurev.med.45.1.325CrossRefPubMed

Hamanaka, R. B., & Mutlu, G. M. (2018). Particulate matter air pollution: Effects on the cardiovascular system. Frontiers in Endocrinology, 9, 680. https://doi.org/10.3389/fendo.2018.00680CrossRefPubMedPubMedCentral

Du, Y., Xu, X., Chu, M., Guo, Y., & Wang, J. (2016). Air particulate matter and cardiovascular disease: The epidemiological, biomedical and clinical evidence. Journal of Thoracic Disease, 8(1), E8–E19. https://doi.org/10.3978/j.issn.2072-1439.2015.11.37CrossRefPubMedPubMedCentral

Januszek, R., Staszczak, B., Siudak, Z., Bartuś, J., Plens, K., Bartuś, S., & Dudek, D. (2020). The relationship between increased air pollution expressed as PM₁₀ concentration and the frequency of percutaneous coronary interventions in patients with acute coronary syndromes-a seasonal differences. Environmental Science and Pollution Research International, 27(17), 21320–21330. https://doi.org/10.1007/s11356-020-08339-6CrossRefPubMedPubMedCentral

Lloyd, A. C., & Cackette, T. A. (2001). Diesel engines: Environmental impact and control. Journal of the Air & Waste Management Association, 51(6), 809–847. https://doi.org/10.1080/10473289.2001.10464315CrossRef

Ramachandra, C., Hernandez-Resendiz, S., Crespo-Avilan, G. E., Lin, Y. H., & Hausenloy, D. J. (2020). Mitochondria in acute myocardial infarction and cardioprotection. eBioMedicine, 57, 102884. https://doi.org/10.1016/j.ebiom.2020.102884CrossRefPubMedPubMedCentral

10.

Mui, D., & Zhang, Y. (2021). Mitochondrial scenario: Roles of mitochondrial dynamics in acute myocardial ischemia/reperfusion injury. Journal of Receptor and Signal Transduction Research, 41(1), 1–5. https://doi.org/10.1080/10799893.2020.1784938CrossRefPubMed

11.

Ide, T., Tsutsui, H., Hayashidani, S., Kang, D., Suematsu, N., Nakamura, K., Utsumi, H., Hamasaki, N., & Takeshita, A. (2001). Mitochondrial DNA damage and dysfunction associated with oxidative stress in failing hearts after myocardial infarction. Circulation Research, 88(5), 529–535.CrossRef

12.

Tsutsui, H., Ide, T., & Kinugawa, S. (2006). Mitochondrial oxidative stress, DNA damage, and heart failure. Antioxidants & Redox Signaling, 8(9–10), 1737–1744. https://doi.org/10.1089/ars.2006.8.1737CrossRef

13.

Sivakumar, B., & Kurian, G. A. (2022). Diesel particulate matter exposure deteriorates cardiovascular health and increases the sensitivity of rat heart towards ischemia reperfusion injury via suppressing mitochondrial bioenergetics function. Chemico-Biological Interactions, 351, 109769. https://doi.org/10.1016/j.cbi.2021.109769CrossRefPubMed

14.

Zheng, P., Liu, J., Mai, S., Yuan, Y., Wang, Y., & Dai, G. (2015). Regulation of signal transducer and activator of transcription 3 and apoptotic pathways by betaine attenuates isoproterenol-induced acute myocardial injury in rats. Human & Experimental Toxicology, 34(5), 538–547. https://doi.org/10.1177/0960327114543936CrossRef

15.

Ravindran, S., Boovarahan, S. R., Shanmugam, K., Vedarathinam, R. C., & Kurian, G. A. (2017). Sodium thiosulfate preconditioning ameliorates ischemia/reperfusion injury in rat hearts via reduction of oxidative stress and apoptosis. Cardiovascular Drugs and Therapy, 31(5–6), 511–524. https://doi.org/10.1007/s10557-017-6751-0CrossRefPubMed

16.

Kaya, M. G., Yalcin, R., Okyay, K., Poyraz, F., Bayraktar, N., Pasaoglu, H., Boyaci, B., & Cengel, A. (2012). Potential role of plasma myeloperoxidase level in predicting long-term outcome of acute myocardial infarction. Texas Heart Institute Journal, 39(4), 500–506.PubMedPubMedCentral

17.

Vogel, B., Siebert, H., Hofmann, U., & Frantz, S. (2015). Determination of collagen content within picrosirius red stained paraffin-embedded tissue sections using fluorescence microscopy. MethodsX, 2, 124–134. https://doi.org/10.1016/j.mex.2015.02.007CrossRefPubMedPubMedCentral

18.

Shanmugam, K., Ravindran, S., Kurian, G. A., & Rajesh, M. (2018). Fisetin Confers Cardioprotection against Myocardial Ischemia Reperfusion Injury by Suppressing Mitochondrial Oxidative Stress and Mitochondrial Dysfunction and Inhibiting Glycogen Synthase Kinase 3β Activity. Oxidative Medicine and Cellular Longevity. https://doi.org/10.1155/2018/9173436CrossRefPubMedPubMedCentral

19.

Barrientos, A., Fontanesi, F., & Díaz, F. (2009). Evaluation of the mitochondrial respiratory chain and oxidative phosphorylation system using polarography and spectrophotometric enzyme assays. Current Protocols in Human Genetics. https://doi.org/10.1002/0471142905.hg1903s63CrossRefPubMedPubMedCentral

20.

Sivakumar, B., & Kurian, G. A. (2021). PM_2.5 from diesel exhaust attenuated fisetin mediated cytoprotection in H9c2 cardiomyocytes subjected to ischemia reoxygenation by inducing mitotoxicity. Drug and Chemical Toxicology. https://doi.org/10.1080/01480545.2021.2003698CrossRefPubMed

21.

Sun, Y. (2009). Myocardial repair/remodelling following infarction: Roles of local factors. Cardiovascular Research, 81(3), 482–490. https://doi.org/10.1093/cvr/cvn333CrossRefPubMed

22.

Talman, V., & Ruskoaho, H. (2016). Cardiac fibrosis in myocardial infarction-from repair and remodeling to regeneration. Cell and Tissue Research, 365(3), 563–581. https://doi.org/10.1007/s00441-016-2431-9CrossRefPubMedPubMedCentral

23.

Frangogiannis, N. G. (2014). The inflammatory response in myocardial injury, repair, and remodelling. Nature Reviews Cardiology, 11(5), 255–265. https://doi.org/10.1038/nrcardio.2014.28CrossRefPubMedPubMedCentral

24.

Wu, L., Woudstra, L., Dam, T. A., Germans, T., van Rossum, A. C., Niessen, H., & Krijnen, P. (2021). Electrocardiographic changes are strongly correlated with the extent of cardiac inflammation in mice with Coxsackievirus B3-induced viral myocarditis. Cardiovascular Pathology: The Official Journal of the Society for Cardiovascular Pathology, 54, 107367. https://doi.org/10.1016/j.carpath.2021.107367CrossRef

25.

Carreira, R. S., Lee, P., & Gottlieb, R. A. (2011). Mitochondrial therapeutics for cardioprotection. Current Pharmaceutical Design, 17(20), 2017–2035. https://doi.org/10.2174/138161211796904777CrossRefPubMedPubMedCentral

26.

Oka, T., Hikoso, S., Yamaguchi, O., Taneike, M., Takeda, T., Tamai, T., Oyabu, J., Murakawa, T., Nakayama, H., Nishida, K., Akira, S., Yamamoto, A., Komuro, I., & Otsu, K. (2012). Mitochondrial DNA that escapes from autophagy causes inflammation and heart failure. Nature, 485(7397), 251–255. https://doi.org/10.1038/nature10992CrossRefPubMedPubMedCentral

27.

Zhen, L., Zhao, Q., Lü, J., Deng, S., Xu, Z., Zhang, L., Zhang, Y., Fan, H., Chen, X., Liu, Z., Gu, Y., & Yu, Z. (2020). miR-301a-PTEN-AKT signaling induces cardiomyocyte proliferation and promotes cardiac repair post-MI. Molecular Therapy: Nucleic Acids, 22, 251–262. https://doi.org/10.1016/j.omtn.2020.08.033CrossRefPubMedPubMedCentral

Title: PM2.5 Exposure Lowers Mitochondrial Endurance During Cardiac Recovery in a Rat Model of Myocardial Infarction
Authors: Bhavana Sivakumar
Gino A. Kurian
Publication date: 01-06-2022
Publisher: Springer US
Keyword: Myocardial Infarction
Published in: Cardiovascular Toxicology / Issue 6/2022
Print ISSN: 1530-7905
Electronic ISSN: 1559-0259
DOI: https://doi.org/10.1007/s12012-022-09737-7

ACC 2024 Congress Coverage

Year in Review: Heart failure and cardiomyopathies

Heart Failure Video

Watch this official video from ACC.24. Dr. Biykem Bozkurt discusses last year's major advances in heart failure and cardiomyopathies.

Watch now

Keynote webinar | Spotlight on medication adherence

Springer Medicine

PM_2.5 Exposure Lowers Mitochondrial Endurance During Cardiac Recovery in a Rat Model of Myocardial Infarction

Abstract

ACC 2024 Congress Coverage

Year in Review: Heart failure and cardiomyopathies

Semaglutide benefits people with type 2 diabetes and obesity-related heart failure

Incentivised to exercise

New intervention for STEMI-related cardiogenic shock

» View more highlights on the ACC 2024 congress hub page

Keynote webinar | Spotlight on medication adherence

Springer Medicine

Abstract

Please log in to get access to this content

Other articles of this Issue 6/2022

NPAS4 Polymorphisms Contribute to Coronary Heart Disease (CHD) Risk

Exosomes Derived from Senescent Endothelial Cells Contain Distinct Pro-angiogenic miRNAs and Proteins

Correlation Between Glycated Hemoglobin (HbA1c) and Post-Systolic Index Measured by Speckle-Tracking Echocardiography in Patients with Non-apparent Coronary Artery Disease

Exosomes Derived from Mesenchymal Stem Cells Ameliorate the Progression of Atherosclerosis in ApoE−/− Mice via FENDRR

Interplay of Obesity, Ethanol, and Contaminant Mixture on Clinical Profiles of Cardiovascular and Metabolic Diseases: Evidence from an Animal Study

Exercise Training Attenuates Cardiac Vulnerability and Promotes Cardiac Resistance to Isoproterenol-Induced Injury Following Hookah Smoke Inhalation in Male Rats: Role of Klotho and Sirtuins

ACC 2024 Congress Coverage

Year in Review: Heart failure and cardiomyopathies

Semaglutide benefits people with type 2 diabetes and obesity-related heart failure

Incentivised to exercise

New intervention for STEMI-related cardiogenic shock

» View more highlights on the ACC 2024 congress hub page