The study is the first evidence that when blood leaks into the nervous system, the blood protein contributes to the neurons’ inability to repair themselves. The research team studied three types of spinal cord injuries in mice and rats which resulted in cellular and vascular damage, and leakage of fibrinogen from the blood vessels. Once injured, neurons cannot be repaired because of various inhibitors that are present in the brain and the spinal cord after damage, which results in a patient’s paralysis.
“Our study shows that fibrinogen directly affects neurons by inhibiting their ability for repair,” said Katerina Akassoglou, Ph.D., assistant professor in University of California, San Diego Health Sciences´ (UCSD) Department of Pharmacology.
Fibrinogen – contained in the blood which leaks at the site of injury – begins the process of inhibiting axonal growth by binding to the beta 3 integrin receptor. This binding, in turn, induces the activation of another receptor on the neuronal cells, called the epidermal growth factor receptor. When the second receptor is activated, it inhibits the axonal growth. Other inhibitors have been identified that use the same epidermal growth factor receptor, but this is the first blood-derived inhibitor that has been found.
The discovery may open the door to a possible strategy to improving recovery after spinal cord injury by discovering a way to block activation of neuronal receptors by fibrinogen. Identifying the specific inhibitors that impede the repair process could provide ways to regenerate and connect the damaged nerves and initiate recovery from paralysis after spinal cord injury. “Inhibiting the damaging effects of fibrinogen on neurons may potentially facilitate repair in the nervous system after injury” said Akassoglou.
MEDICA.de; Source: University of California, San Diego Health Sciences