Pentraxin 3 mediates early inflammatory response and EMT process in human tubule epithelial cells induced by PM2.5.

ABSTRACT

Pentraxin 3 (PTX3) is a multifunctional molecule that mainly expressed in response to proinflammatory stimuli under physiological and pathological conditions. It is produced in tubule epithelial cells that is involved in the innate immune response and inflammatory reactions in the kidney. However, its role in fine particulate matter (PM2.5)-induced renal injury associated with inflammation remains to be investigated. As a result of PM2.5 exposure, the levels of interleukin (IL)-1ß, IL-6 and tumor necrosis factor (TNF)-α levels were increased in HK-2 cells. Notably, the mesenchymal phenotypes with migratory abilities of HK-2 cells were found following PM2.5 exposure. The elevated expressions of PTX3 mRNA and protein in response to PM2.5 were tested by RT-PCR and Western blotting respectively. Further determinate the role of PTX3 by siRNA showed lack of PTX3 could increase IL-6 production and promote epithelial-mesenchymal transition (EMT) process, as evidenced by decreased expressions of E-cadherin, and increased expressions of N-cadherin and α-SMA in HK-2 cells following PM2.5 exposure. Our study indicates that PTX3 mediates early inflammatory response and EMT in PM2.5-exposed HK-2 cells, suggesting a counter-regulatory role of PTX3 in the early course of tubule cell injury induced by PM2.5.