Innovative Cellular Bridges Show Promise for Spinal Cord Injury Repair

Recent advancements in spinal cord injury research indicate that utilizing specific cells within the body's smallest blood vessels may offer a novel approach to repair damaged spinal cords. Scientists have identified a method involving the introduction of a recombinant protein at the site of spinal cord injuries in mice, which appears to facilitate the creation of 'cellular bridges' by altering the behavior of pericytes, a type of cell that surrounds blood vessels.

In experiments, researchers observed that when these pericytes were exposed to a particular growth-factor protein, their shape transformed, leading them to produce some molecules while inhibiting others. This process resulted in the formation of structures that aid in the regeneration of axons--the elongated projections of nerve cells responsible for transmitting signals. The treated mice exhibited signs of axon regrowth and regained mobility in their hind limbs following a single injection of the growth factor.

These findings may extend beyond spinal cord injuries, suggesting potential applications in treating brain injuries, strokes, and neurodegenerative disorders. Researchers emphasize the significance of restoring blood vessel integrity in enhancing neurological recovery after spinal cord trauma.

Spinal cord injuries are particularly devastating, not only disrupting communication across the injury site but also compromising the surrounding vascular structures. Previous studies suggested that these pericytes might hinder recovery; however, recent insights indicate that their properties can change in the presence of specific proteins, such as platelet-derived growth factor BB (PDGF-BB). In cancer studies, targeting PDGF-BB signaling has been a strategy to inhibit tumor blood supply, but in this context, it appears to facilitate recovery.

Investigators noted that pericytes, known for their adaptability, respond positively to changes in their environment, including the presence of PDGF-BB. This adaptability suggested a strategy for enhancing the vascular support necessary for axon regeneration post-injury. Initial imaging studies showed that pericytes migrate into injury sites but do not initially promote the necessary growth of functional blood vessels.

In controlled lab environments, researchers created a layer of pericytes and introduced PDGF-BB, then placed sensory neurons on top. The results demonstrated that axons grew significantly, approaching levels seen under normal conditions. It was revealed that PDGF-BB alone was insufficient for this outcome; the combination of pericytes and the growth factor reorganized fibronectin, a critical protein for tissue repair, allowing cells to adopt more elongated shapes that facilitate axon growth.

To enhance the clinical relevance of these findings, the team also tested human pericytes exposed to PDGF-BB, which similarly stimulated neuron growth, suggesting a broad applicability of this approach across species. In further animal studies, a single dose of PDGF-BB was administered seven days after injury, equivalent to approximately nine months in human terms. The results indicated significant axon regeneration and improved motor control in treated mice.

Moreover, the treatment led to reduced sensitivity to non-painful stimuli, indicating a decrease in neuropathic pain, often a consequence of spinal cord injuries. Analysis of inflammatory markers during the repair process suggested that PDGF-BB not only promotes axon regeneration but also mitigates inflammation.

Future research will delve into the optimal timing for PDGF-BB administration, the ideal concentration for treatment, and the potential for a time-released delivery system. This groundbreaking research opens new avenues for therapeutic strategies that could improve outcomes for individuals suffering from spinal cord injuries.