Retracted : Long noncoding RNA MEG3 deteriorates inflammatory damage by downregulating microRNA‐101a

Valvulopathy is a familiar heart disease, which fearfully harms the health of the body. We studied the effects and mechanism of long noncoding RNA maternally expressed gene 3 (lncMEG3) on MVICs cell in inflammatory damage. Cell Counting Kit‐8 and flow cytometry were respectively used to detect the effect of tumor necrosis factor α (TNF‐α), MEG3 and microRNA (miR)‐101a on cell viability and apoptosis. Moreover, MEG3 and miR‐101a expression were changed by cell transfection and investigated by reverse transcription‐quantitative polymerase chain reaction. Furthermore, Western blot was used to investigate the levels of Bax, pro‐caspase‐3, cleaved‐caspase‐3, pro‐caspase‐9, cleaved‐caspase‐9, interleukin (IL)‐1β, IL‐6 and related‐proteins of cell pathways. Otherwise, the levels of IL‐1β and IL‐6 were also investigated by enzyme‐linked immunosorbent assay kit. Reactive oxygen species (ROS) was examined by ROS assay. We found TNF‐α caused inflammatory damage and upregulated MEG3. MEG3 was overexpressed and silenced in cells. Besides, MEG3 deteriorated inflammatory damage. Furthermore, MEG3 negatively regulated miR‐101a and miR‐101a mimic could reverse the effect of pc‐MEG3. Besides, MEG3 enhanced the JNK and NF‐κB pathways by downregulating miR‐101a. In conclusion, MEG3 deteriorated cell inflammatory damage by downregulating miR‐101a via JNK and NF‐κB pathways.