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Suppression of PTPN6 exacerbates aluminum oxide nanoparticle-induced COPD-like lesions in mice through activation of
Xiaobo Li1, Hongbao Yang2, Shenshen Wu1
1Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Dingjiaqiao 87, Nanjing, 210009, China.
Background:
Inhaled nanoparticles can deposit in the deep lung where they interact with pulmonary cells. Despite numerous studies on pulmonary nanotoxicity, detailed molecular mechanisms of specific nanomaterial-induced lung injury have yet to be identified.
Results:
Using whole-body dynamic inhalation model, we studied the interactions between aluminum oxide nanoparticles (Al2O3 NPs) and the pulmonary system in vivo. We found that seven-day-exposure to Al2O3 NPs resulted in emphysema and small airway remodeling in murine lungs, accompanied by enhanced inflammation and apoptosis. Al2O3 NPs exposure led to suppression of PTPN6 and phosphorylation of STAT3, culminating in increased expression of the apoptotic marker PDCD4. Rescue of PTPN6 expression or application of a STAT3 inhibitor, effectively protected murine lungs from inflammation and apoptosis, as well as, in part, from the induction of chronic obstructive pulmonary disease (COPD)-like effects.
Conclusion:
In summary, our studies show that inhibition of PTPN6 plays a critical role in Al2O3 NPs-induced COPD-like lesions.
Insights
Aluminum oxide nanoparticles (Al2O3 NPs) cause lung injury by suppressing PTPN6, leading to inflammation and COPD-like effects. Restoring PTPN6 protects against these nanoparticle-induced lung damages.
Area of Science:
- Nanotoxicology
- Pulmonary Medicine
- Molecular Biology
Background:
- Inhaled nanoparticles deposit in the deep lung, interacting with pulmonary cells.
- Molecular mechanisms of nanomaterial-induced lung injury remain unclear.
Purpose of the Study:
- Investigate the in vivo interactions between aluminum oxide nanoparticles (Al2O3 NPs) and the pulmonary system.
- Elucidate the molecular mechanisms underlying Al2O3 NP-induced lung injury.
Main Methods:
- Whole-body dynamic inhalation model in murine lungs.
- Analysis of inflammation, apoptosis, and gene expression (PTPN6, STAT3, PDCD4).
- Intervention with PTPN6 expression rescue and STAT3 inhibitor.
Main Results:
- Seven-day Al2O3 NP exposure induced emphysema, airway remodeling, inflammation, and apoptosis.
- Al2O3 NPs suppressed PTPN6 and phosphorylated STAT3, increasing PDCD4 expression.
- PTPN6 rescue or STAT3 inhibition mitigated inflammation, apoptosis, and COPD-like effects.
Conclusions:
- PTPN6 inhibition is critical in Al2O3 NP-induced chronic obstructive pulmonary disease (COPD)-like lesions.
- Targeting PTPN6 or STAT3 pathways offers potential therapeutic strategies for nanoparticle lung injury.
