LAUSR

Secondary pathogenesis following primary mechanical damage to the spinal cord is believed to be the ultimate reason for the limitation of currently available therapies. Precisely, the complex cascade of secondary events-mediated scar formation is the sole hurdle in the recovery process due to its inhibitory effect on axonal regeneration, plasticity, and remyelination. Neutrophils initiate this secondary injury along with other extracellular matrix components such as matrix metalloproteinase (MMPs), and chondroitin sulfate proteoglycans (CSPGs). Together, they mediate inflammation, necrosis, apoptosis, lesion, and scar formation at the injury site. Activated neutrophil releases several proteases, cytokines, and chemokines that cause complete tissue destruction. Thus, neutrophil activation and infiltration in the acute phase of injury act as a roadmap for inducing tissue destruction. MMPs, are extracellular proteolytic enzymes that degrade the ECM proteins, increases vascular permeability, and are predominantly released by neutrophils. These MMPs, in turn, cleave NG2 proteoglycan, a subtype of CSPG, into the active form. This active or shed form is involved in both the fibrotic as well as glial scar formation. Since neutrophils and ECM components are closely associated with each other in pathological conditions. Herein, we emphasize the interaction of neutrophils and their influence on ECM protein expression during the acute and chronic phases to identify a promising targets for designing a therapeutic approach in spinal cord injury.