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J Int Med Res ; 48(5): 300060520918476, 2020 May.
Artigo em Inglês | MEDLINE | ID: mdl-32397779

RESUMO

OBJECTIVE: To explore the function and mechanism of long noncoding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in bronchopulmonary dysplasia. METHODS: Alveolar epithelial cell line BEAS-2B was used as the cell model. The role of MALAT1 and microRNA miR-129-5p in regulating cellular viability and migration were examined by using the CCK-8 and Transwell assays, respectively, in vitro. The luciferase reporter assay and real-time (RT)-PCR were performed to confirm that miR-129-5p was a target of MALAT1. ELISA was conducted to validate MALAT1 and show that miR-129-5p regulated the gene encoding high-mobility group protein 1 (HMGB1). RESULTS: Overexpression of MALAT1 significantly promoted cellular viability, whereas miR-129-5p had the opposite effect. miR-129-5p was shown to be a target of MALAT1, and HMGB1 could be upregulated by MALAT1 overexpression or miR-129-5p inhibition. CONCLUSION: MALAT1 reduced the expression of miR-129-5p, promoting the viability of cells and blocking the development of bronchopulmonary dysplasia. In addition, MALAT1 increased the expression of HMGB1, which contributed to inflammation as the disease progressed.


Assuntos
Células Epiteliais Alveolares/patologia , Displasia Broncopulmonar/genética , Proteína HMGB1/genética , MicroRNAs/metabolismo , RNA Longo não Codificante/metabolismo , Células Epiteliais Alveolares/efeitos dos fármacos , Displasia Broncopulmonar/sangue , Displasia Broncopulmonar/diagnóstico , Displasia Broncopulmonar/patologia , Estudos de Casos e Controles , Linhagem Celular , Movimento Celular/efeitos dos fármacos , Movimento Celular/genética , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/genética , Humanos , Recém-Nascido de Baixo Peso , Recém-Nascido , Recém-Nascido Prematuro , Pulmão/diagnóstico por imagem , MicroRNAs/antagonistas & inibidores , RNA Longo não Codificante/genética , Tomografia Computadorizada por Raios X
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