Perinatal nicotine vaping exposure induces pro-myofibroblastic phenotype in rat bone marrow-derived mesenchymal stem cells
View abstract on PubMed
Summary
This summary is machine-generated.Perinatal electronic-cigarette (e-cig) vaping with nicotine alters bone marrow cells, impairing lung repair. This suggests vaping may increase chronic lung disease risk, similar to smoking.
Area Of Science
- Pulmonology
- Stem Cell Biology
- Toxicology
Background
- Perinatal nicotine exposure from smoking increases chronic lung disease (CLD) risk.
- Nicotine affects bone marrow-derived mesenchymal stem cells (BMSCs), crucial for lung repair.
- Electronic-cigarette (e-cig) use, including by pregnant women, is rising, but its effect on BMSCs is unknown.
Purpose Of The Study
- To investigate if perinatal e-cig nicotine exposure adversely affects BMSCs.
- To determine if e-cig exposure induces a pro-myofibroblastic phenotype in BMSCs.
- To assess the impact on BMSC proliferation, migration, and wound healing capacity.
Main Methods
- Pregnant rats were exposed to fresh air, e-cig vehicle, or e-cig with nicotine.
- Offspring BMSCs were isolated at postnatal day 21.
- Assessed BMSC proliferation, migration, wound healing, and expression of Wnt, PPARγ, and myogenic markers via immunoblotting.
Main Results
- Perinatal e-cig exposure significantly decreased BMSC proliferation, migration, and wound healing.
- Increased expression of Wnt signaling intermediates (β-catenin, LEF-1) and myogenic markers (fibronectin, αSMA, calponin).
- Decreased expression of PPARγ signaling intermediates (PPARγ, ADRP, C/EBPα).
Conclusions
- Perinatal e-cig exposure induces a pro-myofibroblastic phenotype in BMSCs.
- Exposed BMSCs exhibit impaired injury-repair potential.
- Suggests vaping may confer similar chronic lung disease susceptibility as smoking.

