Spinal cord injury (SCI) is a chronic condition that affects signaling in the nervous system by damaging important components, such as neurons. When injury occurs, excessive thrombin is released. However, if protease-activated receptor 1 (PAR1) is removed, studies have shown that there is a possibility for regeneration of necessary aspects in the spinal cord. A critical part of nervous tissue is the myelin sheath, which covers axons to help deliver signals both within the central nervous system and throughout the body. Myelin, and many other aspects of the nervous system, are largely made up of lipids. In injury, the myelin sheath can experience severe degradation. While the importance of lipids in this model is known, their interaction with PAR1 is yet to be discovered. Apolipoprotein E (ApoE) is an important carrier of these lipids and their transport mechanisms in injury could prove important in the SCI PAR1 deletion model. Assessment of this process was completed by comparing the presence of different cell types (oligodendrocyte precursor cells, astrocytes, and neurons) and their colocalization to ApoE in wild type mice (PAR1 +/+) as well as PAR1 knockouts (PAR1 -/-). This analysis identified that PAR1 deletion resulted in an increase in presence of oligodendrocyte precursor cells, GFAP+ astrocytes, and neurons. This leads to the belief that removal of PAR1 improves functional recovery and increases ApoE expression.
