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Published on: January 7, 2019
MiR-4763-3p accelerates lipopolysaccharide-induced cardiomyocyte apoptosis and inflammatory response by targeting
Lei Yang1, Qian Dai2, Xiaoming Bao3
1Department of Cardiac Surgery, Liaocheng People's Hospital, Liaocheng, 252000 Shandong China.
Abstract:
In order to investigate miR-4763-3p and associated genes' roles in myocarditis, AC16 cell line was divided into LPS + miR-4763-3p inhibitor, LPS + NC inhibitor, LPS + miR-4763-3p inhibitor + si-IL10RA and NC groups, and Q-PCR was used to find out whether miR-4763-3p was expressed; Targetscan, Genecards, and MiRDB were used to estimate the miR-4763-3p target; Targetscan was used to display binding sites. Western blot assay was undertaken to detect Bax, Bcl-2, and IL10RA expression. Proliferation and apoptosis were processed using CCK8 and the flow cytometry assay, respectively. Migration and invasion were confirmed utilizing Transwell test. ELISA assay was processed to show the content of IL-6, IL-1ß, IL-10 and TGF-ß in the cell culture supernatant. After being exposed to LPS, cardiomyocyte cells expressed more miR-4763-3p. MiR-4763-3p inhibitor accelerated proliferation, migration and invasion behavior, while it also decreased apoptosis rate in LPS-treated cardiomyocyte cells. MiR-4763-3p inhibitor attenuated the inflammatory response by up-regulating Bax expression and down-regulating Bcl-2 level in LPS-treated cardiomyocyte cells. In cardiomyocyte cells treated with LPS, MiR-4763-3p expression was elevated. si-IL10RA The miR-4763-3p inhibitor restored its effects. MiR-4763-3p accelerates lipopolysaccharide-induced cardiomyocyte apoptosis and inflammatory response by targeting IL10RA, which might be a potential target for myocarditis.
Insights
MicroRNA-4763-3p exacerbates lipopolysaccharide-induced myocarditis by promoting cardiomyocyte apoptosis and inflammation. Inhibiting miR-4763-3p may offer a therapeutic strategy for myocarditis.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Immunology
Background:
- Myocarditis is an inflammatory heart condition with significant morbidity.
- MicroRNAs (miRNAs) play crucial roles in cardiovascular diseases, but their specific functions in myocarditis remain underexplored.
- Understanding the molecular mechanisms underlying myocarditis is essential for developing targeted therapies.
Purpose of the Study:
- To investigate the role of microRNA-4763-3p (miR-4763-3p) in lipopolysaccharide (LPS)-induced myocarditis.
- To identify the molecular targets and pathways regulated by miR-4763-3p in cardiomyocytes.
- To evaluate the therapeutic potential of targeting miR-4763-3p in a cellular model of myocarditis.
Main Methods:
- AC16 cardiomyocyte cell line treated with LPS and transfected with miR-4763-3p inhibitors or control sequences.
- Quantitative PCR (Q-PCR) for gene expression analysis.
- Western blot for protein expression (Bax, Bcl-2, IL10RA).
- Cell proliferation (CCK8), apoptosis (flow cytometry), migration, and invasion assays (Transwell).
- ELISA for inflammatory cytokines (IL-6, IL-1ß, IL-10, TGF-ß).
Main Results:
- LPS exposure significantly increased miR-4763-3p expression in cardiomyocytes.
- Inhibition of miR-4763-3p accelerated cell proliferation, migration, and invasion while reducing apoptosis in LPS-treated cells.
- miR-4763-3p inhibition modulated inflammatory responses by upregulating Bax and downregulating Bcl-2.
- miR-4763-3p was found to target IL10RA, and its inhibition restored effects when IL10RA was silenced.
- miR-4763-3p inhibition attenuated the inflammatory response and protected cardiomyocytes from LPS-induced damage.
Conclusions:
- miR-4763-3p promotes lipopolysaccharide-induced cardiomyocyte apoptosis and inflammation by targeting IL10RA.
- Inhibition of miR-4763-3p demonstrates protective effects against myocarditis in vitro.
- miR-4763-3p represents a potential therapeutic target for managing myocarditis.
