• MALAT1 knockdown protects from bronchial/tracheal smooth muscle cell injury via regulation of microRNA-133a/ryanodine receptor 2 axis

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    • Keywords


      Asthma; apoptosis; inflammation response; MALAT1; microRNA-133a; ryanodine receptor 2

    • Abstract


      Asthma has significant impacts on living quality particularly in children. Long noncoding RNA (lncRNA)MALAT1 plays a crucial role in neonatal respiratory diseases. Meanwhile, MALAT1 knockdown could induceviability and attenuate apoptosis of airway-related cells. However, the role of MALAT1 in neonatal asthma,asthma-related cell, and its possible mechanism is unclear. This study aims to investigate MALAT1 level inasthma and to identify the effects of MALAT1 on bronchial/tracheal smooth muscle cells (B/TSMCs).Newborn asthma modeling rat was constructed by introducing ovalbumin (OVA). MALAT1 levels in tissues orB/TSMCs were determined by RT-qPCR. Exogenous changes of MALAT1, RyR2 or miR-133a in B/TSMCswere fulfilled by cell transfection; cell apoptosis was measured by using Cell Death Detection ELISA kit andHochest33342; IL-6, TNF-alpha and IL-1beta level was detected by using corresponding ELISA kit; ryanodinereceptor 2 (RyR2) mRNA and miR-133a level was determined by RT-qPCR; cleaved caspase-3 (c-caspase-3)and RyR2 expression was detected by Western blot; luciferase reporter assay was performed to confirm thetarget regulation of miR-133a on RyR2. We found that MALAT1 was significantly upregulated in trachealtissues of newborn asthma modeling rats. In MALAT1-silenced or -overexpressed B/TSMCs, we found asynchronous change of cell apoptosis, inflammatory factor secretion (IL-6, TNF-alpha, and IL-1beta) or RyR2 level,but a reverse change of miR-133a level with MALAT1. Besides, MALAT1 induced B/TSMCs apoptosis andinflammation increase could be partially reversed when RyR2 was silenced or when miR-133a was overexpressed.The luciferase reporter assay confirmed that RyR2 is a direct target gene of miR-133a in B/TSMCs.Finally, we conclude that MALAT1 knockdown could protect from B/TSMCs injury via regulating miR-133a/RyR2 axis.

    • Author Affiliations



      1. Department of Pediatric Internal Medicine, Xian Yang Central Hospital, Xianyang 712000, People’s Republic of China
      2. Department of Laboratory Medicine, Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang 712000, People’s Republic of China
    • Dates

  • Journal of Biosciences | News

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