MiR-200a improves respiratory distress syndrome in newborn rabbits via the Wnt/β-catenin signaling pathway

H. Kang, C.-G. Liu, C. Hu, H.-Y. Wang, X.-H. Wang

Department of Neonatal Pediatrics, Shaanxi Provincial People’s Hospital, Xi’an, China. 2220476783@qq.com

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• Respiratory Medicine

OBJECTIVE: The aim of this study was to investigate the effect of micro-ribonucleic acid (miR)-200a on respiratory distress syndrome (RDS) in newborn rabbits by regulating the Wnt/β-catenin signaling pathway.

MATERIALS AND METHODS: In this work, newborn rabbits aged three days were selected from our laboratory as research objects. The messenger RNA (mRNA) and protein expression levels of miR-200a, β-catenin and interleukin-10 (IL-10) in blood samples of healthy newborn rabbits and newborn rabbits with RDS were determined by fluorescence quantitative Polymerase Chain Reaction (PCR) and Western blotting, respectively. Lentivirus-packaged plasmids containing miR-200a were then injected into newborn rabbits suffering from RDS. After 2 d, the mRNA and protein expression levels of miR-200a, β-catenin and IL-10 in blood samples of newborn rabbits in different treatment groups were measured. Meanwhile, lung sections were collected from newborn rabbits in different treatment groups. After that, the sections were observed via hematoxylin and eosin (H&E) staining. At the same time, lung coefficient of newborn rabbits in different treatment groups was also measured.

RESULTS: Compared with healthy newborn rabbits, the mRNA and protein expression levels of miR-200a and IL-10 in the blood of newborn rabbits with RDS decreased significantly (p<0.05), while β-catenin increased markedly (p<0.05). The mRNA and protein expression levels of β-catenin and IL-10 in newborn RDS rabbits with miR-200a over-expression and knockout were detected as well. The results revealed that lowly expressed miR-200a could remarkably promote the expression level of β-catenin, whereas inhibiting the expression of IL-10. However, highly expressed miR-200a could significantly inhibit the expression level of β-catenin and promote the expression level of IL-10. H&E staining results manifested that miR-200a knockout markedly promoted the increase of pulmonary alveoli with increased lung coefficients. However, the up-regulation of miR-200a could reduce lung coefficients and remarkably improve RDS.

CONCLUSIONS: MiR-200a regulates RDS in newborn rabbits by regulating the Wnt/β-catenin signaling pathway.

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