Articles written in Journal of Biosciences

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


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      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.

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