GSE190934
Recombinant FGF10-induced de novo alveologenesis in neonatal mice after hyperoxia exposure is associated with enhanced AT2's resident mesenchymal cell niche activity
Recombinant FGF10 improved hemodynamic measurements and alveologenesis. Alveolosphere assays indicate that the activity of rMC-Sca1Pos is negatively impacted by HYX and partially rescued by FGF10 treatment. scRNAseq results identified clusters expressing Fgf10, Fgf7, Pdgfra, Axin2 which could represent the rMC niche cells for the AT2 stem cells. In this syudy, we demonstrate that FGF10 administration is curative for BPD and identified a subpopulation of rMC-Sca1Pos niche cells which could represent its cellular target. Overall design: In this study, we used a well-established mouse BPD model.C57BL/6J mice were maintained in two groups in NOX (21% O2) and HYX (85% O2) from P0 to P8. Next, We used FGF10 recombinant protein intraperitoneally at three different time intervals (P8-P14, P22-P28 and P36-P42) following HYX. We carried out hemodynamic measurements, morphometry analysis and IF at day 45. scRNAseq between rMC-Sca1Pos isolated from NOX and HYX were also carried out to analyze transcriptional changes in NOX vs. HYX in terms of resident mesenchymal niche activity after injury.