Overexpression of lncRNA TCTN2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injury

Spinal cord injury (SCI) often leads to neuronal apoptosis, a process where nerve cells die, contributing to neurological damage. However, autophagy, a cellular self-cleaning process, can help mitigate this damage by preventing apoptosis. This study explores how a long non-coding RNA called TCTN2 affects both apoptosis and autophagy in SCI. The researchers found that TCTN2 levels are reduced in SCI, while a microRNA called miR-216b is increased. By increasing TCTN2, they could reduce neuron apoptosis and trigger autophagy. TCTN2 appears to regulate miR-216b, promoting autophagy and reducing apoptosis through the miR-216b–Beclin-1 pathway. In a rat model of SCI, increasing TCTN2 improved neurological function. This suggests that TCTN2 can enhance autophagy, thereby reducing neuronal apoptosis and alleviating the effects of spinal cord injury.

• 1
  TCTN2 expression is decreased in spinal cord tissues of rats with SCI and in oxygen–glucose deprivation (OGD)-induced hypoxic SY-SH-5Y cells, while miR-216b is up-regulated in these conditions.
• 2
  Overexpression of TCTN2 reduces neuronal apoptosis by inducing autophagy in SY-SH-5Y cells subjected to OGD, and TCTN2 negatively regulates miR-216b.
• 3
  TCTN2 promotes autophagy to repress apoptosis through the miR-216b–Beclin-1 pathway, and overexpression of TCTN2 improves neurological function in the SCI rat model.