Misoprostol attenuates neonatal cardiomyocyte proliferation through Bnip3, perinuclear calcium signaling, and inhibition of glycolysis

Systemic hypoxia resulting from preterm birth, altered lung development, and cyanotic congenital heart disease is known to impede the regulatory and developmental pathways in the neonatal heart. While the molecular mechanisms are still unknown, hypoxia induces aberrant cardiomyocyte proliferation, which may be initially adaptive, but can ultimately program the heart to fail in early life. Recent evidence suggests that the prostaglandin E1 analogue, misoprostol, is cytoprotective in the hypoxia-exposed neonatal heart by impacting alternative splicing of the Bcl-2 family member Bnip3, resulting in the generation of a variant lacking the third exon (Bnip3 ΔExon3 or small Nip; sNip).

Source: Journal of Molecular and Cellular Cardiology - July 3, 2020 Category: Cytology Authors: Matthew D. Martens, Jared T. Field, Nivedita Seshadri, Chelsea Day, Donald Chapman, Richard Keijzer, Christine A. Doucette, Grant M. Hatch, Adrian R. West, Tammy L. Ivanco, Joseph W. Gordon Source Type: research