Knockdown of LncRNA MEG3 promotes damage of vascular endothelial cells induced by vibration.

Hand-arm vibration syndrome (HAVS) is caused by long-term exposure to hand-transmitted vibration (HTV), and its pathogenesis has not been elucidated fully. We explored the molecular mechanism of HAVS and provided clues and a theoretical basis for the early prevention and treatment of HAVS. After vibration, samples were collected from the plasma of human workers, plasma of rat tails, and human umbilical vein endothelial cells (HUVECs). ELISAs were used to measure the expression of vasoactive factors. Cell Counting Kit-8 and electron microscopy were used to detect cell damage. Flow cytometry was employed to detect apoptosis. Real-time reverse transcription-polymerase chain reaction was used to measure the expression of long non-coding RNAs (lncRNAs). Western blotting was used to measure the expression of apoptosis-related proteins. Vibration could cause cell damage, apoptosis, and changes in the expression vasoactive factors and lncRNAs. The lncRNA maternally expressed gene 3 (MEG3) had a significant regulatory effect on cell damage, apoptotic proteins, and vascular regulatory factors in the HUVEC damage induced by vibration, as shown by the further decrease in viability and aggravation of injury after knockdown of MEG3 expression in HUVECs treated with vibration. Expression of vasoactive factors and apoptosis-related proteins was changed after interfering with MEG3 expression. In conclusion, vibration can affect the expression of vasoactive factors and lncRNA, and cause damage to vascular endothelial cells. MEG3 may be involved in the inflammatory damage to vascular endothelial cells induced by vibration.