FGF6, Mir302d and Mir19b promote cardio-myocyte proliferation

SCHARN A; BAUZÁ MDR; SIMONIN AJ; CIMBARO FS; FERRER P; CROTTOGINI AJ; BELAICH MN; OLEA FD; LOCATELLI P

Congreso; Reunión Anual de Sociedades de Biociencias; 2024

Cardiovascular disease is the leading cause of mortality worldwide, being myocardial infarction with significant cardiomyocyte (CM) loss one of its most severe consequences. Among the strategies to overcome this, is to stimulate cell cycle re-entry to promote cell proliferation. Our aim was to assess the in vitro effects of FGF6, miR302d and miR19b overexpression on cell proliferation and angiogenesis in neonatal rat CMs (NRCMs).Methods: NRCMs were transduced with a baculoviral vector encoding FGF6, miR302d and miR19b (Bv-FGF6-miR302d-miR19b) at MOI 200 and the effect of transgene overexpression was evaluated at 2 and 5 days post-transduction (PT). Cell proliferation was assessed by MTS assay, gene expression by RT-qPCR and immunocytochemistry. Angiogenesis was evaluated by tubulogenesis assay at the same time points. Results: Cyclin D1 and cyclin A2 expression were increased in CMs transduced with Bv-FGF6-miR302d-miR19b compared to Bv-Null at 2 days PT (Cyclin D1 fold increase: 2.07±0.78 vs 1.03±0.29, p