Microvesicle-mediated delivery of miR-1343: impact on markers of fibrosis

We previously identified miR-1343 as a potent repressor of TGF-b signaling and fibrosis through the direct attenuation of both canonical TGF-b receptors. Here, we build upon our previous findings to better characterize the function of endogenous miR-1343 in normal biology. CRISPR/Cas9 techniques were used to delete the miR-1343 locus in A549 lung epithelial cells. Loss of miR-1343 was found to impact several processes and genes implicated in fibrosis and known to be TGF-b pathway effectors. These responses are opposite to those we observed previously when miR-1343 was overexpressed in the same cell type. mRNA profiles of 3 independent deletion clones and 3 non-targeted (NT) clones from the same experiment, as well as 3 replicates of non-clonal A549 cells.