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Updated: May 16, 2026

Myocardial Infarction in Neonatal Mice, A Model of Cardiac Regeneration
Published on: May 24, 2016
The Aplnr GPCR regulates myocardial progenitor development via a novel cell-non-autonomous, Gα(i/o)
Sivani Paskaradevan1, Ian C Scott
1Program in Developmental and Stem Cell Biology, The Hospital for Sick Children, 555 University Avenue , Toronto, ON M5G 1X8 , Canada ; Department of Molecular Genetics, University of Toronto , Toronto, ON M5S 1A8 , Canada.
Abstract:
Myocardial progenitor development involves the migration of cells to the anterior lateral plate mesoderm (ALPM) where they are exposed to the necessary signals for heart development to proceed. Whether the arrival of cells to this location is sufficient, or whether earlier signaling events are required, for progenitor development is poorly understood. Here we demonstrate that in the absence of Aplnr signaling, cells fail to migrate to the heart-forming region of the ALPM. Our work uncovers a previously uncharacterized cell-non-autonomous function for Aplnr signaling in cardiac development. Furthermore, we show that both the single known Aplnr ligand, Apelin, and the canonical Gα(i/o) proteins that signal downstream of Aplnr are dispensable for Aplnr function in the context of myocardial progenitor development. This novel Aplnr signal can be substituted for by activation of Gata5/Smarcd3 in myocardial progenitors, suggesting a novel mechanism for Aplnr signaling in the establishment of a niche required for the proper migration/development of myocardial progenitor cells.
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