PhD Scientific Days 2024

Theoretical and Translational Medicine II.

Molecular Mechanism of the Cardioprotective Effect of a Novel ProtectomiR, miR-450a

Előadó neve

Ms. Nagy, Regina Norma, MSc

Neptun code

C1HY9S

Előadó munkahelye

Department of Pharmacology and Pharmacotherapy

Előadó telefonszáma

+36204339806

Előadó e-mail címe

nagy.regina@phd.semmelweis.hu

Az előadás címe

Molecular Mechanism of the Cardioprotective Effect of a Novel ProtectomiR, miR-450a

Szerző(k) neve és munkahelye

Regina N. Nagy¹, András Makkos¹, Márta Szabó¹, Zoltán Bereczki¹, Bence Ágg¹, Rainer Schulz², Anikó Görbe^1,3, Péter Ferdinandy^1,3

1: HUN-REN–SU System Pharmacology Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University
2: Institute of Physiology, Justus-Liebig University of Giessen, Giessen, Germany
3: Pharmahungary Group, Szeged, Hungary

Bemutatás módja

Szóbeli

Szekció

Theoretical and Translational Medicine II.

Language of the presentation

Hungarian

Preferred session

Theoretical and Translational Medicine

Összefoglaló szövege

Introduction: Cardioprotective miRNAs (protectomiRs) are promising therapeutic tools due to their multi-target effects.
Aims: Here, we aimed to validate the cardiocytoprotective effect of protectomiRs identified in a translational porcine model of acute myocardial infarction (AMI), and determine their cardioprotective mechanism.
Method: Selected protectomiR candidates were validated for their cardiocytoprotective effect in primary rat cardiomyocytes. The two miRNA mimics, miR-450a and miR-451, which increased cell survival following transfection at a concentration of 25 nM and subsequent simulated ischemia-reperfusion injury (sI/R), were further validated in the human cardiomyocyte cell line, AC16. Transfection of AC16 cells with 25, 50, or 100 nM miR-450a mimic, miR-451 mimic, or a negative control miRNA was followed by 16 hours of simulated ischemia and 2 hours of reperfusion. Cell survival was then quantified. For the most potent candidate, miR-450a, target prediction was performed in pigs, rats, and humans. To assess the potential mechanism in cardioprotection, we selected the target genes with cardiac gene expression and performed GO enrichment and KEGG pathway analysis in all three species.
Results: MiR-451 did not increase cell survival following sI/R in AC16 cells. MiR-450a mimic at 25 nM could reverse cell death in AC16 cells. MiR-450a has 3987 predicted mRNA targets in pigs, 4279 in rats, and 8328 in humans. Of these, 607 genes are expressed in all three species. A total of 421 common enriched GO terms were revealed in all three species, while KEGG pathway analysis revealed 13 common pathways, which may play a role in the cardioprotective mechanism.
Conclusion: MiR-450a is a potent protectomiR with cross-species translational value in terms of cardioprotective mechanisms.
Funding: This study was supported by the National Research, Development and Innovation Office of Hungary (NVKP-16-1-2016-0017 National Heart Program, OTKA-FK 134751). Project no. RRF-2.3.1-21-2022-00003 has been implemented with the support provided by the European Union. This project has received funding from HUN-REN Hungarian Research Network. The 2020-1.1.5-GYORSÍTÓSÁV-2021-00011 project was funded by the Ministry for Innovation and Technology with support from the National Research Development and Innovation Fund. RNN was supported by the SE 250+ Excellence PhD Scholarship.

University

Semmelweis University

Supervisor

Dr. Anikó Görbe

Publication of my abstract

I do not give consent to the publication of my abstract on the website of the congress.

Kind

Szabad

Status

elfogadva

Accepted presentation method

szóbeli

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

6888

Start

11:45

End

11:55