Login Register Cart 0
Generic placeholder image

Protein & Peptide Letters

Editor-in-Chief

ISSN (Print): 0929-8665
ISSN (Online): 1875-5305

Back
Journal Home About Journal Editorial Board Journal Insight Current Issue Volumes/Issues
Subscribe
Research Article

miR-490-3p Alleviates Cardiomyocyte Injury via Targeting FOXO1

Author(s): Jin Jiang, Jian Xu and Huifang Tang*

Volume 29, Issue 11, 2022

Published on: 06 October, 2022

Page: [917 - 924] Pages: 8

DOI: 10.2174/0929866529666220819120736

Price: $65

Abstract

Background: MicroRNA-490-3p (miR-490-3p) plays a role in the pathogeneses of a variety of cardiovascular diseases. Bioinformatic analysis showed that miR-490-3p was downregulated in the myocardial tissues of mice with myocardial infarction (MI). Nevertheless, the functions and mechanisms of miR-490-3p in MI remain unclear.

Methods: This study used an in-vitro model to investigate the role of miR-490-3p in MI. Human cardiac myocytes (HCMs) were cultured in a hypoxic environment. 3-(4,5)-Dimethylthiahiazo (-zy1)- 3,5-di-phenytetrazoliumromide (MTT) assay and flow cytometry were used to detect cell viability and apoptosis. The expression levels of forkhead box O1 (FOXO1) and miR-490-3p were detected by quantitative real-time PCR and Western blot. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), lactate dehydrogenase (LDH), cardiac troponin I (cTnI), and creatine kinase MB (CK-MB) were detected by enzyme-linked immunosorbent assay (ELISA). The targeted relationship between miR-490-3p and FOXO1 3’UTR was determined by a dual-luciferase reporter gene assay.

Results: miR-490-3p was significantly down-regulated in hypoxia-induced HCM cells, while FOXO1 was markedly up-regulated. miR-490-3p overexpression inhibited HCM cell inflammatory responses and injury after hypoxia treatment. FOXO1 was validated to be a direct target of miR- 490-3p, and its overexpression weakened the effects of miR-490-3p on cell viability, apoptosis, as well as inflammatory responses.

Conclusion: miR-490-3p alleviates cardiomyocyte injury via targeting FOXO1 in MI.

Keywords: Myocardial, infarction, Hypoxia, Cardiomyocyte, MiR-490-3p, FOXO1

« Previous Next »
[1]
Anderson, J.L.; Morrow, D.A. Acute myocardial infarction. N. Engl. J. Med., 2017, 376(21), 2053-2064.
[http://dx.doi.org/10.1056/NEJMra1606915] [PMID: 28538121]
[2]
Reed, G.W.; Rossi, J.E.; Cannon, C.P. Acute myocardial infarction. Lancet, 2017, 389(10065), 197-210.
[http://dx.doi.org/10.1016/S0140-6736(16)30677-8] [PMID: 27502078]
[3]
Harrington, D.H.; Stueben, F.; Lenahan, C.M. ST elevation myocardial infarction and non-ST elevation myocardial infarction. Crit. Care Nurs. Clin. North Am., 2019, 31(1), 49-64.
[http://dx.doi.org/10.1016/j.cnc.2018.10.002] [PMID: 30736935]
[4]
Somaschini, A.; Astuti, M.; Cordone, S.; Ghione, M.; Buscaglia, E.; Cornara, S.; Bellone, P. An unusual case of syncope due to silent coronary vasospasm. Cardiospace., 2022, 1(1), 11-16.
[5]
Mudaliar, H.; Rayner, B.; Billah, M.; Kapoor, N.; Lay, W.; Dona, A.; Bhindi, R. Remote ischemic preconditioning attenuates EGR-1 expression following myocardial ischemia reperfusion injury through activation of the JAK-STAT pathway. Int. J. Cardiol., 2017, 228, 729-741.
[http://dx.doi.org/10.1016/j.ijcard.2016.11.198] [PMID: 27888751]
[6]
Small, E.M.; Frost, R.J.A.; Olson, E.N. MicroRNAs add a new dimension to cardiovascular disease. Circulation, 2010, 121(8), 1022-1032.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.109.889048] [PMID: 20194875]
[7]
Bartel, D.P. MicroRNAs. Cell, 2004, 116(2), 281-297.
[http://dx.doi.org/10.1016/S0092-8674(04)00045-5] [PMID: 14744438]
[8]
Song, Y.; Zhang, C.; Zhang, J.; Jiao, Z.; Dong, N.; Wang, G.; Wang, Z.; Wang, L. Localized injection of miRNA-21-enriched extracellular vesicles effectively restores cardiac function after myocardial infarction. Theranostics, 2019, 9(8), 2346-2360.
[http://dx.doi.org/10.7150/thno.29945] [PMID: 31149048]
[9]
Zheng, H.F.; Sun, J.; Zou, Z.Y.; Zhang, Y.; Hou, G.Y. MiRNA-488-3p suppresses acute myocardial infarction induced cardiomyocyte apoptosis via targeting ZNF791. Eur. Rev. Med. Pharmacol. Sci., 2019, 23(11), 4932-4939.
[PMID: 31210328]
[10]
Wu, Y.; Mao, Q.; Liang, X. Targeting the MicroRNA-490-3p-ATG4B-autophagy axis relieves myocardial injury in ischemia reperfusion. J. Cardiovasc. Transl. Res., 2020.
[PMID: 32474761]
[11]
Guo, X.; Liu, Y.; Zheng, X.; Han, Y.; Cheng, J. HOTTIP knockdown inhibits cell proliferation and migration via regulating miR-490-3p/HMGB1 axis and PI3K-AKT signaling pathway in ox-LDL-induced VSMCs. Life Sci., 2020, 248, 117445.
[http://dx.doi.org/10.1016/j.lfs.2020.117445] [PMID: 32081664]
[12]
Liu, Y.; Chen, Y.; Tan, L.; Zhao, H.; Xiao, N. Linc00299/miR-490-3p/AURKA axis regulates cell growth and migration in atherosclerosis. Heart Vessels, 2019, 34(8), 1370-1380.
[http://dx.doi.org/10.1007/s00380-019-01356-7] [PMID: 30734057]
[13]
Loi, H.; Boal, F.; Tronchere, H.; Cinato, M.; Kramar, S.; Oleshchuk, O.; Korda, M.; Kunduzova, O. Metformin protects the heart against hypertrophic and apoptotic remodeling after myocardial infarction. Front. Pharmacol., 2019, 10, 154.
[http://dx.doi.org/10.3389/fphar.2019.00154] [PMID: 30873028]
[14]
Spurthi, K.M.; Sarikhani, M.; Mishra, S.; Desingu, P.A.; Yadav, S.; Rao, S.; Maity, S.; Tamta, A.K.; Kumar, S.; Majumdar, S.; Jain, A.; Raghuraman, A.; Khan, D.; Singh, I.; Samuel, R.J.; Ramachandra, S.G.; Nandi, D.; Sundaresan, N.R. Toll like receptor 2 deficiency hyperactivates the FoxO1 transcription factor and induces aging-associated cardiac dysfunction in mice. J. Biol. Chem., 2018, 293(34), 13073-13089.
[http://dx.doi.org/10.1074/jbc.RA118.001880] [PMID: 29929978]
[15]
Anderson, K.M. Discharge clinical characteristics and 60-day readmission in patients hospitalized with heart failure. J. Cardiovasc. Nurs., 2014, 29(3), 232-241.
[http://dx.doi.org/10.1097/JCN.0b013e31828f0d25] [PMID: 23612038]
[16]
Putko, B.N.; Wang, Z.; Lo, J.; Anderson, T.; Becher, H.; Dyck, J.R.B.; Kassiri, Z.; Oudit, G.Y. Circulating levels of tumor necrosis factor alpha receptor 2 are increased in heart failure with preserved ejection fraction relative to heart failure with reduced ejection fraction: Evidence for a divergence in pathophysiology. PLoS One, 2014, 9(6), e99495.
[http://dx.doi.org/10.1371/journal.pone.0099495] [PMID: 24923671]
[17]
Gabisonia, K.; Prosdocimo, G.; Aquaro, G.D.; Carlucci, L.; Zentilin, L.; Secco, I.; Ali, H.; Braga, L.; Gorgodze, N.; Bernini, F.; Burchielli, S.; Collesi, C.; Zandonà, L.; Sinagra, G.; Piacenti, M.; Zacchigna, S.; Bussani, R.; Recchia, F.A.; Giacca, M. MicroRNA therapy stimulates uncontrolled cardiac repair after myocardial infarction in pigs. Nature, 2019, 569(7756), 418-422.
[http://dx.doi.org/10.1038/s41586-019-1191-6] [PMID: 31068698]
[18]
Huang, S.; Frangogiannis, N.G. Anti inflammatory therapies in myocardial infarction: Failures, hopes and challenges. Br. J. Pharmacol., 2018, 175(9), 1377-1400.
[http://dx.doi.org/10.1111/bph.14155] [PMID: 29394499]
[19]
Xu, Y.; Guo, W.; Zeng, D.; Fang, Y.; Wang, R.; Guo, D.; Qi, B.; Xue, Y.; Xue, F.; Jin, Z.; Li, Y.; Zhang, M. Inhibiting miR-205 alleviates cardiac ischemia/reperfusion injury by regulating oxidative stress, mitochondrial function, and apoptosis. Oxid. Med. Cell. Longev., 2021, 2021, 1-17.
[http://dx.doi.org/10.1155/2021/9986506] [PMID: 34306321]
[20]
Bejerano, T.; Etzion, S.; Elyagon, S.; Etzion, Y.; Cohen, S. Nanoparticle delivery of miRNA-21 mimic to cardiac macrophages improves myocardial remodeling after myocardial infarction. Nano Lett., 2018, 18(9), 5885-5891.
[http://dx.doi.org/10.1021/acs.nanolett.8b02578] [PMID: 30141949]
[21]
Xiao, Y.; Zhao, J.; Tuazon, J.P.; Borlongan, C.V.; Yu, G. MicroRNA-133a and myocardial infarction. Cell Transplant., 2019, 28(7), 831-838.
[http://dx.doi.org/10.1177/0963689719843806] [PMID: 30983393]
[22]
Gao, F.; Kataoka, M.; Liu, N.; Liang, T.; Huang, Z.P.; Gu, F.; Ding, J.; Liu, J.; Zhang, F.; Ma, Q.; Wang, Y.; Zhang, M.; Hu, X.; Kyselovic, J.; Hu, X.; Pu, W.T.; Wang, J.; Chen, J.; Wang, D.Z. Therapeutic role of miR-19a/19b in cardiac regeneration and protection from myocardial infarction. Nat. Commun., 2019, 10(1), 1802.
[http://dx.doi.org/10.1038/s41467-019-09530-1] [PMID: 30996254]
[23]
Puthanveetil, P.; Wan, A.; Rodrigues, B. FoxO1 is crucial for sustaining cardiomyocyte metabolism and cell survival. Cardiovasc. Res., 2013, 97(3), 393-403.
[http://dx.doi.org/10.1093/cvr/cvs426] [PMID: 23263330]
[24]
Yu, W.; Chen, C.; Cheng, J. The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy. ESC Heart Fail., 2020, 7(6), 3497-3504.
[http://dx.doi.org/10.1002/ehf2.13065] [PMID: 33089967]
[25]
Ronnebaum, S.M.; Patterson, C. The FoxO family in cardiac function and dysfunction. Annu. Rev. Physiol., 2010, 72(1), 81-94.
[http://dx.doi.org/10.1146/annurev-physiol-021909-135931] [PMID: 20148668]
[26]
Qin, X.D.; Liu, L. Loss of microRNA-27a induces cardiac dysfunction through activating FoxO1. Eur. Rev. Med. Pharmacol. Sci., 2019, 23(13), 5941-5948.
[PMID: 31298345]
[27]
Qiu, Z.; Wang, L.; Mao, H.; Xu, F.; Sun, B.; Lian, X.; Wang, J.; Kong, F.; Wang, L.; Chen, Y. MiR 370 inhibits the oxidative stress and apoptosis of cardiac myocytes induced by hydrogen peroxide by targeting FOXO1. Exp. Ther. Med., 2019, 18(4), 3025-3031.
[http://dx.doi.org/10.3892/etm.2019.7908] [PMID: 31555385]
[28]
Cai, B.; Wang, N.; Mao, W.; You, T.; Lu, Y.; Li, X.; Ye, B.; Li, F.; Xu, H. Deletion of FoxO1 leads to shortening of QRS by increasing Na+ channel activity through enhanced expression of both cardiac NaV1.5 and β3 subunit. J. Mol. Cell. Cardiol., 2014, 74, 297-306.
[http://dx.doi.org/10.1016/j.yjmcc.2014.06.006] [PMID: 24956219]

Rights & Permissions Print Cite
Article Metrics
1
© 2024 Bentham Science Publishers | Privacy Policy