LncRNA CRNDE modulates cardiac progenitor cells' proliferation and migration via the miR-181a/LYRM1 axis in hypoxia.

Abstract

BackgroundThe cardiac progenitor cells provide a valuable method for myocardial infarction related heart failure therapies. But cardiac progenitor cell quickly loses the proliferation abilities during the myocardial infarction. In this paper, we aim to explore the role of lncRNA CRNDE in the modulation of cardiac progenitor cell reproduction and migration.MethodsCardiac progenitor cells were isolated from neonatal adult Sprague-Dawley rats by removing the heart and homogenizing the tissue. Various siRNAs and RNA mimics were co-transfected to the cells. A list of characterization methods, including qRT-PCR, Western blotting, luciferase assay, CCK-8 assay, and EdU incorporation assay, were utilized to verify the roles and interactions of CRNDE, miR-181a, and LYRM1 in cardiac progenitor cells’ proliferation and migration potentials.ResultsLncRNA CRNDE expressions were substantially promoted in the CoCl2-related hypoxia cardiac progenitor cell model. CRNDE suppression inhibited cardiac progenitor cell reproduction and migration under hypoxic conditions. The miR-181a-inhibitor restored the reproduction and migration potentials of cardiac progenitor cells after CRNDE knockdown in hypoxia. LYR motif containing 1 (LYRM1) was a target of miR-181a, and miR-181a negatively modulated its expressions. LYRM1 knockdowns inhibited miR-181a-inhibitor's protective effects for cardiac progenitor cell functions in hypoxia.ConclusionsOur experiments and analysis demonstrated that CRNDE could modulate cardiac progenitor cell proliferation and migration potentials via the miR-181a/LYRM1 axis in hypoxia.