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

Abstract

Abstract. 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.

Perfluorocarbon reduces cell damage from blast injury by inhibiting signal paths of NF-κB, MAPK and Bcl-2/Bax signaling pathway in A549 cells

“…PFC is not soluble, and we can not use it in cell culture. Therefore, we mixed PFC and DMEM at a ratio of 9:1 as previously described [15]. PFC and DMEM were mixed on ice at 21 kHz and 350 W in a transonic analogous ultrasonic unit for 10 sec.…”

“…Moreover, the levels of cytokines, chemokines and other mediators of pulmonary inflammation are reduced by PFC [14]. Our group found that PFC decreased intercellular adhesion caused by lipopolysaccharide (LPS), which induces damage to A549 cells [15]. …”

Long non-coding RNA MALAT1 exacerbates acute respiratory distress syndrome by upregulating ICAM-1 expression via microRNA-150-5p downregulation

“…The primer sequences (Table 1) for MALAT1, miR-150-5p, ICAM-1 and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were designed and synthesized by Shanghai Sangon Biotechnology Co., Ltd. (Shanghai, China). The relative expression of the target gene was calculated using the 2 -ΔΔCt method with GAPDH serving as the internal reference [42][43][44][45].…”

A Functionalized Membrane Layer as Part of a Dressing to Aid Wound Healing

“…Moreover, perfluorocarbon emulsions have been applied to enhance oxygen transport in cell cultures [ 18 ]. The PFC influence on cells such as cell line RINm5F beta cells, rat pancreatic cells, A549 cells, and osteoblasts were assessed [ 19 , 20 , 21 ]. In addition, some authors proposed that the substrates improve oxygenation for the ‘cells’ growth increase.…”