Conclusions
The overexpressed PRMT6 could serve as an inflammation inhibitor, potentially through blocking the NF-κB/p65 pathway in the murine emphysema model.
Methods
Mice were injected with cigarette smoke extract (CSE) or PBS to establish a mice model, intratracheally instilled with overexpressed PRMT6 or negative control vector. Morphometry of lung slides and lung function were measured. We determined the protein expression of PRMT6 and its related histone targets, the activation of NF-κB pathway, the level of tumor necrosis factor α (TNFα) and interleukin-1β (IL-1β).
Results
After PRMT6 overexpression, the morphometry indexes and lung function were improved. Also, the expression of H3K4me3 was decreased. Overexpressed PRMT6 could suppress CSE-induced NF-κB activation and pro-inflammation genes expression. Conclusions: The overexpressed PRMT6 could serve as an inflammation inhibitor, potentially through blocking the NF-κB/p65 pathway in the murine emphysema model.