Fig. 5From: Elk1 enhances inflammatory cell infiltration and exacerbates acute lung injury/acute respiratory distress syndrome by suppressing Fcgr2b transcriptionARDS models have high Elk1 expression, which represses Fcgr2b transcription. Notes A, Immunohistochemistry to examine Elk1 expression in lung tissues of ARDS rats (n = 6/group); B-C, RT-qPCR and western blot to determine Elk1 expression in LPS-induced PMVECs (N = 3); D, RT-qPCR to detect Elk1 and Fcgr2b expression in PMVECs after lentiviral infection and LPS induction (N = 3); E, ChIP-qPCR to assess the binding relationship between Elk1/H3K9me3 and Fcgr2b promoter (N = 3); F, dual-luciferase reporter assay to evaluate the transcriptional regulation of Elk1 to Fcgr2b (N = 3). Differences between two groups were compared using the t-test (A-C, F), and differences among multiple groups were compared using one-way (E) or two-way (D) analysis of variance with Tukey’s post-hoc test. ARDS, acute respiratory distress syndrome; LPS, lipopolysaccharide; PMVECs, pulmonary microvascular endothelial cells; H3K9me3, histone 3 lysine 9 trimethylationBack to article page