Dexamethasone can attenuate the pulmonary inflammatory response via regulation of the lncH19/miR-324-3p cascade

Abstract Objective To investigate lncRNAs and their roles in regulating the pulmonary inflammatory response under dexamethasone (Dex) treatment. Methods IL-1? (10 ng/mL) LPS (1 ?g/mL) was used to construct cell models with A549 cells; performed better against LPS. Different concentrations of Dex were attenuate inflammation induced by IL-1?, its effect assessed via RT-PCR detect cytokine-related mRNA levels, including those IK?-?, IKK?, IL-6, IL-8, TNF-?. Furthermore, ELISA levels cytokines TNF-?, IL-8. quantify lncRNAs, lncMALAT1, lncHotair, lncH19, lncNeat1. LncH19 most closely associated response, which attenuated Dex. Among level lncH19 showed highest increase following treatment 1 10 ?M Therefore, selected for further functional studies. expression inhibited shRNA transduced lentivirus. Cell assays proliferation apoptosis as well RT-PCR, western blot, genes conducted confirm functions lncH19. The predicted target miRNAs hsa-miR-346, hsa-miR-324-3p, hsa-miR-18a-3p, hsa-miR-18b-5p, hsa-miR-146b-3p, hsa-miR-19b-3p, hsa-miR-19a-3p. Following estimation hsa-miR-324-3p consistent patterns NC shlncH19. An miRNA inhibitor transfected into shlncH19 cells, determined RT-PCR. compared hsa-miR-346 hsa-miR-18a-3p subjected ELISA, blotting gene detection validate hsa-miR-324-3p. Results Treatment could effectively response. During this process, significantly increased ( P < 0.05). study. Under or without Dex, inhibition led an proliferation; a decrease apoptosis; protein genes; phosphorylation P65, ICAM-1, VCAM-1; cytokines. Prediction targets validation revealed that miR-346, miR-18a-3p, miR-324-3p negatively correlate Additionally, but reduced miRNAs. miRNAs, markedly downregulated inhibitors. MTS assay apoptosis, thereby attenuating reversed secretion might regulate Conclusion can lncH19/miR-324-3p cascade.