Current issue
Archive
Manuscripts accepted
About the Journal
Editorial office
Editorial board
Section Editors NEW
Abstracting and indexing
Subscription
Contact
Ethical standards and procedures
Most read articles
Instructions for authors
Article Processing Charge (APC)
Regulations of paying article processing charge (APC)
CARDIOLOGY / EXPERIMENTAL RESEARCH
mRNA-103 inhibition attenuates autophagy and inflammation in myocardial infarction by regulating the TLR4 pathway
1
School of Life Science, Northwest University, Xian, China
2
Department of Vascular Surgery, General Hospital of PLA, Beijing, China
3
Department of Cardiology, Affiliated Hospital of Northwest University, Xian, China
4
Department of Cardiology, Xian No. 3 Hospital, Xian, China
5
Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, College of Life Science, Northwest University, Xian, China
6
School of Life Science, Beijing Institute of Technology, Beijing, China
Submission date: 2019-11-09
Final revision date: 2020-01-15
Acceptance date: 2020-01-31
Online publication date: 2020-02-25
Publication date: 2025-02-28
Corresponding author
Kang Cheng
Department of Cardiology Affiliated Hospital of Northwest University Xian No. 3 Hospital 710018 Xian China
Department of Cardiology Affiliated Hospital of Northwest University Xian No. 3 Hospital 710018 Xian China
Arch Med Sci 2025;21(1):266-271
KEYWORDS
TOPICS
ABSTRACT
Introduction:
This investigation determined the cardioprotective activity of mRNA-103 inhibitor against myocardial infarction (MI) and also evaluated its molecular mechanism.
Material and methods:
MI was induced in rats by inducing myocardial ischaemia/reperfusion (I/R), and left ventricular (LV) mRNA-103 (1 × 107 TU) was injected into the myocardium around the infarcted area. The effect of mRNA-103 inhibitor was assessed by determining the levels of myocardial enzymes and cytokines in the serum, the myeloperoxidase (MPO) activity, and the levels of Toll-like receptor 4 (TLR4), nuclear factor k-light-chain enhancer of activated B cells (NF-kB), and MyD88 mRNAs in the myocardial tissues of MI rats. Immunocytochemical analysis and a histopathology study were also performed.
Results:
The levels of myocardial enzymes and cytokines were lower in the mRNA-103 inhibitor-treated group than in the group in which the only treatment was the induction of MI. There was a lower percentage of infarcted area and a lower apoptosis index in the mRNA-103 inhibitor-treated group compared to the MI-only. The levels of TLR4, NF-kB, and MyD88 mRNAs were lower in the myocardial tissues of the mRNA-103 inhibitor-treated group than in the MI-only group. Immunohistochemical analysis revealed that treatment with mRNA-103 inhibitor ameliorated the expression of TLR4 in the myocardial tissues of MI rats.
Conclusions:
The data revealed that inhibition by mRNA-103 protects against myocardial injury in MI rats by regulating the inflammasome pathway.
This investigation determined the cardioprotective activity of mRNA-103 inhibitor against myocardial infarction (MI) and also evaluated its molecular mechanism.
Material and methods:
MI was induced in rats by inducing myocardial ischaemia/reperfusion (I/R), and left ventricular (LV) mRNA-103 (1 × 107 TU) was injected into the myocardium around the infarcted area. The effect of mRNA-103 inhibitor was assessed by determining the levels of myocardial enzymes and cytokines in the serum, the myeloperoxidase (MPO) activity, and the levels of Toll-like receptor 4 (TLR4), nuclear factor k-light-chain enhancer of activated B cells (NF-kB), and MyD88 mRNAs in the myocardial tissues of MI rats. Immunocytochemical analysis and a histopathology study were also performed.
Results:
The levels of myocardial enzymes and cytokines were lower in the mRNA-103 inhibitor-treated group than in the group in which the only treatment was the induction of MI. There was a lower percentage of infarcted area and a lower apoptosis index in the mRNA-103 inhibitor-treated group compared to the MI-only. The levels of TLR4, NF-kB, and MyD88 mRNAs were lower in the myocardial tissues of the mRNA-103 inhibitor-treated group than in the MI-only group. Immunohistochemical analysis revealed that treatment with mRNA-103 inhibitor ameliorated the expression of TLR4 in the myocardial tissues of MI rats.
Conclusions:
The data revealed that inhibition by mRNA-103 protects against myocardial injury in MI rats by regulating the inflammasome pathway.
REFERENCES (25)
1.
Institute of Medicine (US) Committee on Social Security Cardiovascular Disability Criteria. Cardiovascular Disability: Updating the Social Security Listings. Washington (DC): National Academies Press (US); 2010. 7, Ischemic Heart Disease.
2.
Schmidt MR, Pryds K, Bøtker HE. Novel adjunctive treatments of myocardial infarction. World J Cardiol 2014; 6: 434-43.
3.
Kalogeris T, Baines CP, Krenz M, Korthuis RJ. Cell biology of ischemia/reperfusion injury. Int Rev Cell Mol Biol 2012; 298: 229-317.
4.
Yang X, Li Y, Li Y, et al. Oxidative stress-mediated atherosclerosis: mechanisms and therapies. Front Physiol 2017; 8: 600.
5.
Liu J, Wang H, Li J. Inflammation and inflammatory cells in myocardial infarction and reperfusion injury: a double-edged sword. Clin Med Insights Cardiol 2016; 10: 79-84.
6.
Zhang JM, An J. Cytokines, inflammation, and pain. Int Anesthesiol Clin 2007; 45: 27-37.
7.
Yang Y, Lv J, Jiang S, et al. The emerging role of Toll-like receptor 4 in myocardial inflammation. Cell Death Dis 2016; 7: e2234.
8.
Samanta S, Balasubramanian S, Rajasingh S, et al. MicroRNA: a new therapeutic strategy for cardiovascular diseases. Trends Cardiovasc Med 2016; 26: 407-19.
9.
Wang J, Liew OW, Richards AM, Chen YT. Overview of microRNAs in cardiac hypertrophy, fibrosis, and apoptosis. Int J Mol Sci 2016; 17: E749.
10.
Trajkovski M, Hausser J, Soutschek J, et al. Micro-RNAs 103 and 107 regulate insulin sensitivity. Nature 2011; 474: 649-53.
11.
Hilton C, Neville MJ, Karpe F. MicroRNAs in adipose tissue: their role in adipogenesis and obesity. Int J Obes 2013; 37: 325-32.
12.
Fernández-Hernando C, Ramírez CM, Goedeke L, Suárez Y. MicroRNAs in metabolic disease. Arterioscler Thromb Vasc Biol 2013; 33: 178-85.
13.
Torres JL, Novo-Veleiro I, Manzanedo L, et al. Role of microRNAs in alcohol-induced liver disorders and non-alcoholic fatty liver disease. World J Gastroenterol 2018; 24: 4104-18.
14.
Jiang X, Jiang L, Shan A, et al. Targeting hepatic miR-221/222 for therapeutic intervention of nonalcoholic steatohepatitis in mice. EBioMedicine 2018; 37: 307-21.
15.
Kfir-Erenfeld S, Haggiag N, Biton M, Stepensky P, Assayag-Asherie N, Yefenof E. miR-103 inhibits proliferation and sensitizes hemopoietic tumor cells for glucocorticoid-induced apoptosis. Oncotarget 2017; 8: 472-89.
16.
Aman U, Vaibhav P, Balaraman R. Tomato lycopene attenuates myocardial infarction induced by isoproterenol: electrocardiographic, biochemical and anti-apoptotic study. Asian Pac J Trop Biomed 2012; 2: 345-51.
17.
Lim KH, Ko D, Kim JH. Cardioprotective potential of Korean Red Ginseng extract on isoproterenol-induced cardiac injury in rats. J Ginseng Res 2013; 37: 273-82.
18.
Ong SB, Hernández-Reséndiz S, Crespo-Avilan GE, et al. Inflammation following acute myocardial infarction: multiple players, dynamic roles, and novel therapeutic opportunities. Pharmacol Ther 2018; 186: 73-87.
19.
Sedaghat Z, Kadkhodaee M, Seifi B, Salehi E. Inducible and endothelial nitric oxide synthase distribution and expression with hind limb per-conditioning of the rat kidney. Arch Med Sci 2019; 15: 1081-91.
20.
Wang Y, Hu H, Yin J, et al. TLR4 participates in sympathetic hyperactivity post-MI in the PVN by regulating NF-kappaB pathway and ROS production. Redox Biol 2019; 24: 101186.
21.
Kurian GA, Rajagopal R, Vedantham S, Rajesh M. The role of oxidative stress in myocardial ischemia and reperfusion injury and remodeling: revisited. Oxid Med Cell Longev 2016; 2016: 1656450.
22.
Krijnen PA, Nijmeijer R, Meijer CJ, Visser CA, Hack CE, Niessen HW. Apoptosis in myocardial ischaemia and infarction. J Clin Pathol 2002; 55: 801-11.
23.
Tian XF, Cui MX, Yang SW, Zhou YJ, Hu DY. Cell death, dysglycemia and myocardial infarction. Biomed Rep 2013; 1: 341-6.
24.
Gorący J, Kaczmarczyk M, Ciechanowicz A, et al. E-selectin gene haplotypes are associated with the risk of myocardial infarction. Arch Med Sci 2019; 15: 1223-31.
25.
Eken MK, Ersoy GS, Kaygusuz EI, et al. Etanercept protects ovarian reserve against ischemia/reperfusion injury in a rat model. Arch Med Sci 2019; 15: 1104-12.
Share
RELATED ARTICLE
| eISSN: | 1896-9151 |
| ISSN: | 1734-1922 |
We process personal data collected when visiting the website. The function of obtaining information about users and their behavior is carried out by voluntarily entered information in forms and saving cookies in end devices. Data, including cookies, are used to provide services, improve the user experience and to analyze the traffic in accordance with the Privacy policy. Data are also collected and processed by Google Analytics tool (more).
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
