作者: Christina T. Fulton , Tracy X. Cui , Adam M. Goldsmith , Jennifer Bermick , Antonia P. Popova
DOI: 10.1038/S41598-018-35256-Z
关键词: Mesenchymal stem cell 、 Immunology 、 PDGFRA 、 Lung 、 Bronchopulmonary dysplasia 、 Transcriptome 、 WNT2 、 Proinflammatory cytokine 、 MMP3 、 Medicine
摘要: Male sex is a risk factor for development of bronchopulmonary dysplasia (BPD), common chronic lung disease following preterm birth. We previously found that tracheal aspirate mesenchymal stromal cells (MSCs) from premature infants developing BPD show reduced expression PDGFRα, which required normal development. hypothesized MSCs male exhibit pathologic gene profile deficient in PDGFR and its downstream effectors, thereby favoring delayed In discovery cohort 6 7 female infants, we analyzed the transcriptome. A unique signature distinguished all other MSCs. Genes involved development, PDGF signaling extracellular matrix remodeling were differentially expressed. sought to confirm these findings second 13 12 infants. mRNA PDGFRA, FGF7, WNT2, SPRY1, MMP3 FOXF2 significantly lower BPD. BPD, levels proinflammatory CCL2 profibrotic Galectin-1 higher compared not Our support notion sex-specific differences mechanisms