Abstract
Particulate matter exposure has been known as a potential risk for the global burden of disease, such as respiratory and cardiovascular diseases. Accumulating evidence suggests that PM2.5 (particulate matter with a diameter less than 2.5 μm) is associated with increased risk of kidney disease, but the mechanisms underlying the renal injury caused by PM2.5 remain to be elucidated. This study investigated the effects of PM2.5 on human proximal tubular epithelial (HK-2) cells by monolayer and 3D spheroid cultures and explored the potential mechanisms. The typical morphology of HK-2 cells showed epithelial–mesenchymal transition (EMT), resulting in reduced adhesion and enhanced migration after PM2.5 exposure, and was accompanied by decreased E-cadherin expression and increased vimentin and α-SMA expressions. Exposure to PM2.5 in the HK-2 cells could lead to an increase in interleukin-6 (IL-6) levels and cause the activation of signal transducer and activator of transcription 3 (STAT3), which is involved in EMT features of HK-2 cells. Furthermore, blocking IL-6/STAT3 signaling by an IL-6 neutralizing antibody or STAT3 inhibitor was sufficient to reverse PM2.5-induced EMT characteristics of the HK-2 cells. Our study suggests that PM2.5 could induce early renal tubule cell injury, contributing to EMT change, and the induction of IL-6/STAT3 pathway may play an important role in this process.
Highlights
This study aimed to investigate the effects of PM2.5 on human HK-2 cells and examine the role of IL-6/signal transducer and activator of transcription 3 (STAT3) pathway in PM2.5-induced epithelial–mesenchymal transition (EMT)
Enzyme-Linked Immunosorbent Assay (ELISA), and the results showed the IL-6 levels were 2 cells induced by PM2.5 and assessed the expression of STAT3 and phosphorylated significa increased after PM2.5 exposure (Figure 3a)
In order to investigate the role of IL-6 in regulating the EMT of HK-2 cells, we further induced by PM2.5
Summary
Renal injury is associated with tubucells gradually acquire mesenchymal characteristics and lost their epithelial lointerstitial fibrosis, and the reversal of EMT may slow the progression of CKD [17–19]. This study aimed to investigate the effects of PM2.5 on human HK-2 cells and examine the role of IL-6/STAT3 pathway in PM2.5-induced EMT. AHowever, we observed a progressive ance, but those cells treated with increased concentrations of PM2.5 underwent a morphochange in the phenotype of HK-2 cells following exposure to higher levels of PM2.5. Least three three independent changes of HK-2 cells following different concentrations of PM2.5 exposure Theassess effect of PM2.5 on HK-2 cell wound healing was performed to to HK-2 cellswounds hadmigration, increased migratory properties following treatment. Results indicate that PM2.5 could resultofin of HK-2(Figure cells, characterized duced E-cadherin and increased expressions vimentin and α-SMA.
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