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Open AccessArticle

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

1
Department of Internal and Agricultural Medicine, Faculty of Medicine, Jagiellonian University Medical College, 31-121 Cracow, Poland
2
Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow G12 8TA, UK
*
Author to whom correspondence should be addressed.
Academic Editor: Paola Giussani
Int. J. Mol. Sci. 2021, 22(7), 3616; https://doi.org/10.3390/ijms22073616
Received: 5 March 2021 / Revised: 25 March 2021 / Accepted: 29 March 2021 / Published: 31 March 2021
(This article belongs to the Special Issue Sphingolipid Metabolism and Signaling in Diseases)
Sphingosine kinase-1 (Sphk1) and its product, sphingosine-1-phosphate (S1P) are important regulators of cardiac growth and function. Numerous studies have reported that Sphk1/S1P signaling is essential for embryonic cardiac development and promotes pathological cardiac hypertrophy in adulthood. However, no studies have addressed the role of Sphk1 in postnatal cardiomyocyte (CM) development so far. The present study aimed to assess the molecular mechanism(s) by which Sphk1 silencing might influence CMs development and hypertrophy in vitro. Neonatal mouse CMs were transfected with siRNA against Sphk1 or negative control, and subsequently treated with 1 µM angiotensin II (AngII) or a control buffer for 24 h. The results of RNASeq analysis revealed that diminished expression of Sphk1 significantly accelerated neonatal CM maturation by inhibiting cell proliferation and inducing developmental pathways in the stress (AngII-induced) conditions. Importantly, similar effects were observed in the control conditions. Enhanced maturation of Sphk1-lacking CMs was further confirmed by the upregulation of the physiological hypertrophy-related signaling pathway involving Akt and downstream glycogen synthase kinase 3 beta (Gsk3β) downregulation. In summary, we demonstrated that the Sphk1 silencing in neonatal mouse CMs facilitated their postnatal maturation in both physiological and stress conditions. View Full-Text
Keywords: sphingosine kinase-1; sphingosine-1-phosphate; cardiomyocyte; cardiomyocyte hypertrophy; cardiomyocyte maturation; cardiomyocyte proliferation sphingosine kinase-1; sphingosine-1-phosphate; cardiomyocyte; cardiomyocyte hypertrophy; cardiomyocyte maturation; cardiomyocyte proliferation
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MDPI and ACS Style

Jozefczuk, E.; Szczepaniak, P.; Guzik, T.J.; Siedlinski, M. Silencing of Sphingosine kinase 1 Affects Maturation Pathways in Mouse Neonatal Cardiomyocytes. Int. J. Mol. Sci. 2021, 22, 3616. https://doi.org/10.3390/ijms22073616

AMA Style

Jozefczuk E, Szczepaniak P, Guzik TJ, Siedlinski M. Silencing of Sphingosine kinase 1 Affects Maturation Pathways in Mouse Neonatal Cardiomyocytes. International Journal of Molecular Sciences. 2021; 22(7):3616. https://doi.org/10.3390/ijms22073616

Chicago/Turabian Style

Jozefczuk, Ewelina; Szczepaniak, Piotr; Guzik, Tomasz J.; Siedlinski, Mateusz. 2021. "Silencing of Sphingosine kinase 1 Affects Maturation Pathways in Mouse Neonatal Cardiomyocytes" Int. J. Mol. Sci. 22, no. 7: 3616. https://doi.org/10.3390/ijms22073616

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