Fra-2 negatively regulates postnatal alveolar septation by modulating myofibroblast function

Purpose: Compare the transciptome between lung myofibroblasts that contituatively express Fra-2 to control lung myofibroblasts to determine genes that may contribute to regulation of secondary alveolar septation Methods: mRNa sequences from lung myofibroblasts isolated from mutant mice that contituatively express Fra-2 in α-SMA expressing cells (sma-Fra2) were compared to control mice. n=4 in each group Results: 43,432 transcripts wre analyzed and 361 genes were differentially expressed in the smaFra2 mice compared to wild type control. Functional analysis was performed using the Database for Annotation, Visualization and Integrated Discovery. Changes in genes from lung myofibroblasts in smaFra2 mice: genes involved with extracellular matrix and cell adhesion were upregulated; Ectonucleotide pyrophosphatase/phosphodiesterase family member 2 (Enpp2) and LPA receptor1 (LPA1) were downregulated. Coclusion: The secondary alveolar septation defect in smaFra2 mice could be explaned by Fra-2 mediated changes in extracellular matrix and cell adhesion in developing lung myofibroblasts. Genome-wide sequencing of lung myofiblasts that constituatively express Fra-2