FGF10 identifies early lipofibroblast progenitors and controls their fate during embryonic lung development

摘要: Introduction: Lipofibroblasts (LIFs) are lipid-containing fibroblasts found in the late fetal and postnatal lung parenchyma. LIFs assimilate lipids transfer triglycerides to adjacent alveolar epithelial type II cells elaborate surfactant. Aims: Although have been studied lungs, their cellular origin mechanism of differentiation unknown. We aim determine molecular pathway that control fate. Methods: Using Fgf10-LacZ Fgf10iCre mouse lines, we analyzed expression markers Fgf10-positive situ after sorting. In addition, used vivo knockdown FGFR2b ligand activity from E14.5 E18.5 Fgf10 hypomorphs as well vitro models (WI-38, NIH3T3-L1 cell lines primary cultures fibroblasts) test whether FGF10 is capable on acting directly mesenchyme promote differentiation. Results: demonstrated express permanently labeled at embryonic days E11.5 or E15.5 give rise LIFs. reduction led decreased LIF E18.5. culture WI-38 human progenitor adipocyte cells, demonstrate recombinant trigger commitment these adipogenic lineage. Moreover, also antagonizes TGFβ1-induced myofibroblast transdifferentiation cells. Conclusion: Our results essential role signaling formation.