Research Paper Volume 12, Issue 8 pp 6570—6585

Figure 1. Downregulated MALAT1 inhibits apoptosis of HPMECs while decreasing the expression of pro-inflammatory cytokines and adhesion factors. (A) Expression of MALAT1 in peripheral blood samples of healthy controls (n = 46) and patients with ARDS (n = 46), as determined by RT-qPCR. * p < 0.05 vs. peripheral blood samples of healthy controls. (B) Expression of MALAT1 in normal and LPS-treated HPMECs, as determined by RT-qPCR. * p < 0.05 vs. the control cells. (C) Subcellular localization of MALAT1 in HPMECs detected by FISH (400 ×). (D) Expression of MALAT1 in HPMECs transfected with oe-MALAT1 or sh-MALAT1 determined by RT-qPCR. (E) Expression of pro-inflammatory cytokines (IL-6, IL-1β and TNF-α) in HPMECs transfected with oe-MALAT1 or sh-MALAT1 determined by ELISA. (F) Expression of endothelial cell adhesion molecules (E-selectin and ICAM-1) in HPMECs transfected with oe-MALAT1 or sh-MALAT1, as detected by immunofluorescence (× 200). (G) HPMEC apoptosis upon transfection with oe-MALAT1 or sh-MALAT1 detected by TUNEL assay (× 200). (H) Expression of Bcl-2, Bax, cleaved caspase 3 and Caspase3 in HPMECs transfected with oe-MALAT1 or sh-MALAT1 detected by Western blot analysis. * p < 0.05 vs. cells transfected with oe-MALAT1 NC or sh-MALAT1 NC. The data were measurement data and expressed as mean ± standard deviation. The data between two groups were compared using unpaired t-test and those among multiple groups were analyzed by one-way ANOVA, with Tukey's post hoc test. The cell experiment was repeated three times independently.