Inhibition and Role of let-7d in Idiopathic Pulmonary Fibrosis
Pandit KV, Corcoran D, Yousef H, Yarlagadda M, Tzouvelekis A, Gibson KF, Konishi K, Yousem SA, Singh M, Handley D, Richards T, Selman M, Watkins SC, Pardo A, Ben-Yehudah A, Bouros D, Eickelberg O, Ray P, Benos PV, Kaminski N. Inhibition and Role of let-7d in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2010, 182: 220-229. PMID: 20395557, PMCID: PMC2913236, DOI: 10.1164/rccm.200911-1698oc.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCadherinsCells, CulturedDown-RegulationEpithelial CellsHMGA2 ProteinHumansIdiopathic Pulmonary FibrosisIn Situ HybridizationLungMiceMice, Inbred C57BLMicroRNAsPolymerase Chain ReactionPulmonary AlveoliS100 Calcium-Binding Protein A4S100 ProteinsSmad3 ProteinTransforming Growth Factor betaVimentinConceptsIdiopathic pulmonary fibrosisReal-time polymerase chain reactionQuantitative real-time polymerase chain reactionAlveolar epithelial cellsIPF lungsPulmonary fibrosisPolymerase chain reactionLet-7dEpithelial cellsLethal fibrotic lung diseaseAlpha-smooth muscle actinAlveolar septal thickeningMesenchymal markers N-cadherinFibrotic lung diseaseChain reactionLet-7d expressionSeptal thickeningPulmonary functionLung diseaseLung fibrosisEpithelial cell lineIntratracheal administrationIPF tissueProfibrotic effectsClinical trials