JOURNAL OF NEUROTRAUMA, 2017 · DOI: 10.1089/neu.2016.4757 · Published: March 15, 2017
Inflammation is a key process after spinal cord injuries, driven by substances like TNF-α and IL-1β produced by brain cells called astrocytes and microglia. These substances are controlled by RNA binding proteins (RBPs), including human antigen R (HuR). This study found that after spinal cord injury in mice, HuR moves into the cytoplasm of astrocytes, suggesting it becomes active. Blocking HuR reduced the production of inflammatory substances by astrocytes and reduced their ability to attract other immune cells. Therefore, HuR could be a target for therapies to reduce inflammation and secondary tissue damage following CNS injuries.
HuR may be a therapeutic target for blunting secondary tissue injury triggered by the inflammatory response in acute CNS trauma.
HuR is a key modulator of the inflammatory response and may be a therapeutic target for reducing secondary tissue injury in early CNS trauma.
Development of drugs targeting HuR could potentially reduce the recruitment of immune cells and the production of cytokines, leading to less tissue damage.