Perinatal nicotine vaping exposure induces pro-myofibroblastic phenotype in rat bone marrow-derived mesenchymal stem cells.
Publication Year:
2024
PubMed ID:
39059775
Funding Grants:
Public Summary:
Electronic cigarettes (e-cigs) are often marketed as a safer alternative to traditional smoking, but new research shows that vaping during pregnancy may still pose serious risks to a baby’s developing lungs. This study reveals how nicotine exposure from e-cigs can damage a special type of stem cell that helps repair lung tissue—raising concerns about long-term respiratory health in children.
This study focused on bone marrow–derived mesenchymal stem cells (BMSCs), which are essential for healing and regenerating lung tissue after injury. Using a rat model, the authors exposed pregnant mothers to either clean air, e-cig vapor without nicotine, or e-cig vapor with nicotine throughout pregnancy and nursing.
The study found that offsprings exposed to nicotine-containing e-cig vapor had BMSCs that were less able to grow, move, and repair wounds—key functions for tissue regeneration. These cells also showed signs of shifting toward a “pro-fibrotic” state, meaning they were more likely to contribute to scarring rather than healing. This was linked to changes in two important molecular pathways: Wnt signaling (which increased) and PPARγ signaling (which decreased). These pathways are known to influence how stem cells behave and how tissues develop and repair.
Understanding how environmental exposures like nicotine affect stem cell function is critical to developing therapies that can restore or protect organ health. This study highlights the need for public awareness about the risks of vaping during pregnancy and underscores the importance of protecting stem cell health during critical windows of development. It also opens the door to future research on how we might use stem cell–based therapies to reverse or prevent the damage caused by early nicotine exposure.
Scientific Abstract:
Perinatal nicotine exposure via tobacco smoking results in increased proclivity to chronic lung disease (CLD); however, the underlying molecular mechanisms remain incompletely understood. We previously demonstrated that in addition to nicotine's direct effects on the developing lung, there are also adverse molecular alterations in bone marrow-derived mesenchymal stem cells (BMSCs), which are vital to lung injury repair. Whether perinatal nicotine exposure via electronic-cigarette (e-cig) vaping also adversely affects BMSCs is unknown. This is highly relevant due to marked increase in e-cig vaping including by pregnant women. Hypothesizing that perinatal nicotine exposure via e-cig vaping predisposes BMSCs to a pro-myofibroblastic phenotype, pregnant rat dams were exposed to fresh air (control), vehicle (e-cig without nicotine), or e-cig (e-cig with nicotine) daily during pregnancy and lactation. At postnatal day 21, offspring BMSCs were isolated and studied for cell proliferation, migration, wound healing response, and expression of key Wnt and PPARgamma signaling intermediates (beta-catenin, LEF-1, PPARgamma, ADRP and C/EBPalpha) and myogenic markers (fibronectin, alphaSMA, calponin) proteins using immunoblotting. Compared to controls, perinatal e-cig exposure resulted in significant decrease in BMSC proliferation, migration, and wound healing response. The expression of key Wnt signaling intermediates (beta-catenin, LEF-1) and myogenic markers (fibronectin, alphaSMA, calponin) increased significantly, while PPARgamma signaling intermediates (PPARgamma, ADRP, and C/EBPalpha) decreased significantly. Based on these data, we conclude that perinatally e-cig exposed BMSCs demonstrate pro-myofibroblastic phenotype and impaired injury-repair potential, indicating a potentially similar susceptibility to CLD following perinatal nicotine exposure via vaping as seen following parenteral perinatal nicotine exposure.
