Inhibition of TGF-beta1 promotes functional recovery after spinal cord injury

Neurosci Res. 2009 Dec;65(4):393-401. doi: 10.1016/j.neures.2009.08.017. Epub 2009 Sep 8.


Trauma to the spinal cord initiates a series of cellular and biochemical processes that damage both neurons and glia. TGF-beta and its receptors are expressed around the injury site following a spinal cord injury. Here, we report that the intrathecal administration of a neutralizing antibody to TGF-beta1 in rats with thoracic spinal cord contusion results in a significant enhancement of the locomotor recovery. The inhibition of TGF-beta1 suppresses glial scar formation and upregulates microglia/macrophage activation after the injury, presumably providing a favorable environment for restoration of the neural network. Rats treated with the anti-TGF-beta1 antibody exhibited a mild enhancement of growth and/or preservation of axons in the injured spinal cord caudal to the site of contusion. These results support the possibility of using TGF-beta1 inhibitors in the treatment of human spinal cord injuries.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Neutralizing / therapeutic use*
  • Female
  • Immunohistochemistry
  • Macrophage Activation / drug effects
  • Macrophages / immunology
  • Macrophages / metabolism
  • Microglia / immunology
  • Microglia / metabolism
  • Nerve Regeneration / drug effects
  • Nerve Regeneration / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Recovery of Function*
  • Spinal Cord Injuries / drug therapy*
  • Spinal Cord Injuries / immunology
  • Spinal Cord Injuries / metabolism*
  • Transforming Growth Factor beta1 / antagonists & inhibitors*


  • Antibodies, Neutralizing
  • Tgfb1 protein, rat
  • Transforming Growth Factor beta1