Silencing of Sphingosine kinase 1 Affects Maturation Pathways in Mouse Neonatal Cardiomyocytes

Sphingosine kinase-1 (Sphk1) and its product, sphingosine-1-phosphate (S1P) are important regulators of cardiac growth function. Numerous studies have reported that Sphk1/S1P signaling is essential for embryonic development promotes pathological hypertrophy in adulthood. However, no addressed the role Sphk1 postnatal cardiomyocyte (CM) so far. The present study aimed to assess molecular mechanism(s) by which silencing might influence CMs vitro. Neonatal mouse were transfected with siRNA against or negative control, subsequently treated 1 µM angiotensin II (AngII) a control buffer 24 h. results RNASeq analysis revealed diminished expression significantly accelerated neonatal CM maturation inhibiting cell proliferation inducing developmental pathways stress (AngII-induced) conditions. Importantly, similar effects observed Enhanced Sphk1-lacking was further confirmed upregulation physiological hypertrophy-related pathway involving Akt downstream glycogen synthase kinase 3 beta (Gsk3?) downregulation. In summary, we demonstrated facilitated their both