Data Sheet 1_ANKRD22 contributes to NF-κB-associated inflammatory responses in alveolar type II epithelial cells during PM2.5-triggered airway inflammation.docx

RNA sequencing was used to explore the regulatory mechanisms of ANKRD22 in AT-II cells during PM_2.5-induced airway inflammation.</p>Results<p>Our study demonstrated that PM_2.5 promoted ANKRD22 expression in AT-II cells both in vivo and in vitro. PM_2.5-induced inflammation was alleviated in AT-II- ANKRD22^△/△ mice. The expression of IL6, IL8, IL1B, CXCL1, and CXCL2 was downregulated by ANKRD22 siRNA in A549 cells.

Mechanistically, PM_2.5 exposure significantly enhanced the protein expression of P50 and the phosphorylation of IKKβ, IκBα and RELA. Moreover, these PM_2.5-induced changes were markedly attenuated following ANKRD22 deficiency. Similarly, PM_2.5 exposure induced significant upregulation of p52 protein levels and RELB phosphorylation, which were substantially reduced by ANKRD22 knockdown.</p>Conclusion<p>In conclusion, PM_2.5 stimulation promoted the ANKRD22 expression in AT-II cells, thereby contributing to NF-κB-associated inflammatory responses during PM2.5-induced airway inflammation.</p>