OBJECTIVE To explore whether microRNA-615-3p participates in the progression of neonatal acute respiratory distress syndrome (ARDS) by inhibiting differentiation of mesenchymal stem cells (MSCs) to alveolar type II epithelial cells… Click to show full abstract
OBJECTIVE To explore whether microRNA-615-3p participates in the progression of neonatal acute respiratory distress syndrome (ARDS) by inhibiting differentiation of mesenchymal stem cells (MSCs) to alveolar type II epithelial cells (ATII) via Wnt/β-catenin pathway. PATIENTS AND METHODS Expression levels of microRNA-615-3p and inflammatory factors (IL-1, IL-6, IL-8, and TNF-α) in peripheral blood of 24 neonatal ARDS patients and 14 healthy newborns were detected by qRT-PCR (quantitative Real-Time Polymerase Chain Reaction). MSCs were isolated from bone marrow of mice and identified by flow cytometry. The effect of microRNA-615-3p on regulating the differentiation of MSCs to ATII was analyzed. After altering expressions of microRNA-615-3p and DKK1 by plasmids transfection, Wnt/β-catenin pathway-related genes were detected by Western blot. RESULTS Higher expression levels of microRNA-615-3p and inflammatory factors (IL-1, IL-6, IL-8, and TNF-α) were observed in peripheral blood of neonatal ARDS patients than those of healthy newborns. ATII-specific genes were upregulated, and inflammatory factors were downregulated after the microRNA-615-3p knockdown in MSCs. Moreover, expressions of Wnt/β-catenin pathway-related genes were downregulated after the microRNA-615-3p overexpression, which was partially reserved by the DKK1 knockdown. CONCLUSIONS Overexpressed microRNA-615-3p promoted ARDS development through inhibiting differentiation of MSCs to ATII via Wnt/β-catenin pathway.
               
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