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In-silico analyses of medical data and microRNA databases predicted a probable relationship between miRNA-34a (miR-34a), mitogen-activated protein kinase 1 (ERK), and kruppel like factor 4 (Klf4). Parallel to in silico outcomes, right here, we reveal that intra-tracheal instillation of lipopolysaccharides (LPS) to mice enhanced miR-34a phrase in lung macrophages. Inhibition of miR-34a notably improved lung histology, whereas over-expression of miR-34a worsened the lung damage phenotype.
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