Abstract
Objective To illustrate the role of tanshinone IIA (TSN) in regulating cardiac structure and function following myocardial infarction (MI) and the involvement of miR-205-3p in TSN-induced antifibrosis effect on ventricular remodeling. Patients and Methods. One hundred MI patients were randomly assigned into two groups, and they were treated with TSN (TSN group, n = 50) or conventional therapy (control group, n = 50). Plasma levels of miR-205-3p and TGF-β1 were detected in each patient. Echocardiography was conducted in each patient at post-MI 1 day, 2 weeks, and 4 weeks, respectively, for recording LVIDd (left ventricular internal-diastolic diameter), LVIDs (left ventricular internal-systolic diameter), and LVEF (left ventricular ejection fraction). The interaction between miR-205-3p and TGF-β1 was examined by the RNA-Binding Protein Immunoprecipitation (RIP) assay. After induction of TGF-β1 and/or 10 μL of TSN in cardiac fibroblasts, relative levels of miR-205-3p, Col1a1, and Col3a1 were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Results Compared with the control group, miR-205-3p and TGF-β1 were downregulated in plasma of MI patients in the TSN group. In the TSN group, LVIDd and LVIDs were reduced, and EF was enhanced at 2 weeks and 4 weeks compared with that at post-MI 1 day. miR-205-3p could negatively interact with TGF-β1. TSN induction abolished the regulatory effects of TGF-β1 on downregulating miR-205-3p and upregulating Col1a1 and Col3a1 in cardiac fibroblasts. Conclusions Through upregulating miR-205-3p and downregulating TGF-β1, TSN alleviates cardiac fibrosis and improves ventricular remodeling following MI.
Highlights
The treatment of acute myocardial infarction (AMI) has been well concerned owing to its high incidence and mortality [1]
Tanshinone IIA (TSN) has been extensively applied in the clinical treatment of vascular diseases, and its promising application has been reported in treating coronary disease, hypertension, cardiac ischemiareperfusion injury, and arrhythmia [5]
It is reported that miR-29 participates in the development of cardiac fibrosis at post-MI via regulating cardiac fibroblast functions. miR-205 is located on chromosome 1q, which is abnormally expressed in many types of tumors and involved in regulating tumor cell behaviors [8, 9]
Summary
To illustrate the role of tanshinone IIA (TSN) in regulating cardiac structure and function following myocardial infarction (MI) and the involvement of miR-205-3p in TSN-induced antifibrosis effect on ventricular remodeling. Plasma levels of miR-205-3p and TGF-β1 were detected in each patient. After induction of TGF-β1 and/or 10 μL of TSN in cardiac fibroblasts, relative levels of miR-205-3p, Col1a1, and Col3a1 were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Compared with the control group, miR-205-3p and TGF-β1 were downregulated in plasma of MI patients in the TSN group. In the TSN group, LVIDd and LVIDs were reduced, and EF was enhanced at 2 weeks and 4 weeks compared with that at post-MI 1 day. TSN induction abolished the regulatory effects of TGF-β1 on downregulating miR-205-3p and upregulating Col1a1 and Col3a1 in cardiac fibroblasts. Through upregulating miR-205-3p and downregulating TGF-β1, TSN alleviates cardiac fibrosis and improves ventricular remodeling following MI
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
