Abstract 224: Primary Human Cells Isolated From Atria and Bone Marrow Exhibit Comparable Anti-fibrotic Cell Phenotypes Upon Transfection With MicroRNA-301a
There are many cell types that can contribute to cardiac fibrosis including atrial fibroblasts (AFs) and bone marrow-derived progenitor cells (MPCs). We have previously shown that MPCs display a myofibroblast phenotype in vitro which is linked to altered microRNA(miR)-301a expression, a miR affiliated with maintaining proliferation in numerous cell types. We have also shown that miR-301a influences a dichotomous phenotype in primary human MPCs isolated from patients undergoing open heart surgery. As both MPCs and AFs display a dichotomous phenotype where each cell type displays a phenotype that pathologically contributes to fibrosis, we transfected both MPCs and AFs with miR-301a. AFs were also isolated from patients undergoing open heart surgery. We observed decreases in levels of both mRNA and protein of collagen I, non-muscle myosin IIA, and EDA-fibronectin. These proteins are expressed in myofibroblasts, the cell type predominantly responsible for causing cardiac fibrosis. In addition, transfection of miR301a caused both cell types to increase proliferation, which was analyzed using MTT proliferation assays. These results indicate that miR-301a could be influencing a non-fibrotic phenotype, which could prove useful in cell therapy trials where progenitor cells are injected into scar tissue in order to help heal patients who have suffered from a myocardial infarction. Over-expressing miR-301a in cells used could prevent them from differentiating into pro-fibrotic phenotypes and encourage their proliferation, thereby potentiating their efficacy.
Author Disclosures: A.L. Müller: None. D.H. Freed: None.
- © 2015 by American Heart Association, Inc.