Details

Autor(en) / Beteiligte

• CAO, LU
• LI, CHUN-SUN
• CHANG, YAN
• LIANG, ZHI-XIN
• CHEN, LIANG-AN

Titel

The effects of perfluorocarbon on ICAM-1 expression in LPS-induced A549 cells and the potential mechanism

Ist Teil von

• Molecular medicine reports, 2016-04, Vol.13 (4), p.3700-3708

Ort / Verlag

Greece: D.A. Spandidos

Erscheinungsjahr

2016

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• Acute lung injury (ALI)/ARDS is a critical clinical syndrome with high mortality, and the effective therapeutic methods for the treatment remain limited. Previous studies have indicated that liquid ventilation with perfluorocarbon (PFC) may be advantageous over conventional mechanical ventilation in the treatment of ALI/ARDS. Additionally, PFC inhibits the inflammatory response caused by ALI/ARDS. However, the anti-inflammatory mechanism remains to be completely elucidated. In the present study, the aim was to determine the anti-inflammatory mechanism of PFC and the association with microRNA (miR). PFC was used to modulate LPS-induced A549 cells, with the cells divided into four groups: Untreated control group; LPS group, treated with 10 µg/ml LPS; LPS+PFC group, treated with 10 µg/ml LPS and PFC; and PFC group, treated with PFC alone. The intercellular adhesion molecule-1 (ICAM-1) mRNA and protein expression levels of each group were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting, respectively. A549 cells were transfected with miR-17-3p mimics, miR-17-3p inhibitors or negative controls to observe the alterations in the anti-inflammatory effects of PFC. A dual luciferase reporter gene assay was used to determine whether ICAM-1 is a target gene of miR-17-3p. PFC was observed to attenuate the mRNA and protein expression levels of ICAM-1 in LPS-induced A549 cells, with no significant effect on the untreated A549 cells. miR-17-3p was demonstrated to be regulated by PFC. Transfection with miR-17-3p mimics enhanced the anti-inflammatory effects of PFC, whereas the miR-17-3p inhibitor weakened the anti-inflammatory effects of PFC at early time points. To conclude, the current study indicates that ICAM-1 was a target gene of miR-17-3p, and PFC has anti-inflammatory effects. Additionally, the present study is the first report, to the best of our knowledge, that PFC is able to attenuate ICAM-1 expression in LPS-induced A549 cells by increasing miR-17-3p expression.