European review for medical and pharmacological sciences · 2019
Effects of MiR-26a on respiratory distress syndrome in neonatal rats via the wnt/β-catenin signaling pathway.
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Kornaszewska Marta, Ogorzelec Natalia, Kowalewski Mariusz, Fedorowski Artur, Suwalski Piotr, Stec Sebastian
Аннотация
OBJECTIVE: Micro ribonucleic acids (miRNAs) are crucial to post-transcriptional regulation of the gene expression. Whether miR-26a affects respiratory distress syndrome (RDS) in neonatal rats through the Wnt/β-catenin signaling pathway was investigated in this study.
PATIENTS AND METHODS: The neonatal rat model of RDS was established, and the expressions of miR-26a and glycogen synthase kinase-3β (GSK-3β) in RDS in neonatal rats and their correlation were analyzed. The cascade relationship between miR-26a and the Wnt/β-catenin signaling pathway and the influence of miR-26a on the expression of inflammatory cytokines were subsequently verified. Finally, the influences of miR-26a on the expressions of important markers, receptor for advanced glycation endproducts (RAGE), high mobility group box 1 (HMGB1), and plasminogen activator inhibitor-1 (PAI-1), through the Wnt/β-catenin signaling pathway were analyzed.
RESULTS: Compared with those in normal tissues, the expression of miR-26a in lung tissues of neonatal rats with RDS was significantly decreased (p<0.05), while the expression of GSK-3β messenger RNAs (mRNAs) was notably increased (p<0.01), and the GSK-3β expression was negatively correlated with the miR-26a expression (r=-0.6693, p=0.0064). In addition, miR-26a mimics significantly inhibited the GSK-3β protein expression and activated the Wnt/β-catenin signaling pathway. Moreover, miR-26a could reduce the expressions of tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and IL-6, as well as RAGE, HMGB1, and PAI-1.
CONCLUSIONS: MiR-26a can affect inflammatory responses and markers through the Wnt/β-catenin signaling pathway in neonatal rats with RDS.
PATIENTS AND METHODS: The neonatal rat model of RDS was established, and the expressions of miR-26a and glycogen synthase kinase-3β (GSK-3β) in RDS in neonatal rats and their correlation were analyzed. The cascade relationship between miR-26a and the Wnt/β-catenin signaling pathway and the influence of miR-26a on the expression of inflammatory cytokines were subsequently verified. Finally, the influences of miR-26a on the expressions of important markers, receptor for advanced glycation endproducts (RAGE), high mobility group box 1 (HMGB1), and plasminogen activator inhibitor-1 (PAI-1), through the Wnt/β-catenin signaling pathway were analyzed.
RESULTS: Compared with those in normal tissues, the expression of miR-26a in lung tissues of neonatal rats with RDS was significantly decreased (p<0.05), while the expression of GSK-3β messenger RNAs (mRNAs) was notably increased (p<0.01), and the GSK-3β expression was negatively correlated with the miR-26a expression (r=-0.6693, p=0.0064). In addition, miR-26a mimics significantly inhibited the GSK-3β protein expression and activated the Wnt/β-catenin signaling pathway. Moreover, miR-26a could reduce the expressions of tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and IL-6, as well as RAGE, HMGB1, and PAI-1.
CONCLUSIONS: MiR-26a can affect inflammatory responses and markers through the Wnt/β-catenin signaling pathway in neonatal rats with RDS.