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FOXF1 transcription factor promotes lung regeneration after partial pneumonectomy
Craig Bolte1,2, Hannah M Flood3,4, Xiaomeng Ren3,4
1Center for Lung Regenerative Medicine, Cincinnati Children's Research Foundation, Cincinnati, Ohio, USA. Craig.Bolte@cchmc.org.
Scientific Reports
|September 8, 2017
Summary
Forkhead box F1 (FOXF1) transcription factor is crucial for lung regeneration. FOXF1 deficiency in endothelial cells impairs lung repair by affecting cell proliferation and gene expression, highlighting its role in this process.
Area of Science:
- Pulmonary Medicine
- Developmental Biology
- Molecular Biology
Background:
- Forkhead box F1 (FOXF1) is essential for lung development, homeostasis, and injury repair.
- The specific role of FOXF1 in lung regeneration remains largely unexplored.
Purpose of the Study:
- To investigate the function of FOXF1 in endothelial cells during lung regeneration.
- To identify FOXF1 target genes involved in the lung regeneration process.
Main Methods:
- Partial pneumonectomy was performed on mice with endothelial cell-specific Foxf1 deficiency (PDGFb-iCre/Foxf1 fl/+).
- Endothelial cell proliferation was assessed, and RNA sequencing was performed on sorted endothelial cells.
- Chromatin immunoprecipitation sequencing (ChIP-seq) was used to identify direct FOXF1 targets.
Main Results:
- Endothelial cell-specific Foxf1 deficiency significantly reduced endothelial cell proliferation in regenerating lungs.
- Foxf1 deficiency led to delayed lung regeneration, evidenced by reduced respiratory volume.
- Gene expression analysis revealed FOXF1 regulates genes involved in extracellular matrix remodeling (e.g., Timp3, Adamts9) and cell cycle progression (e.g., Cdkn1a, Cdkn2b).
- ChIP-seq confirmed FOXF1 directly targets regulatory regions of Cd44, Cdkn1a, and Cdkn2b.
Conclusions:
- FOXF1 is a critical regulator of lung regeneration following partial pneumonectomy.
- FOXF1 promotes lung regeneration by directly controlling the transcription of genes vital for extracellular matrix remodeling and cell cycle progression in endothelial cells.
