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Arginine depletion via Arginase-1 as a key mechanism of M2- macrophage-induced neuroprotection after spinal cord injury. (R-8162)
Worldwide, over two million people are affected by a spinal cord injury (SCI). This devastating disorder is a major cause of morbidity, mortality and reduced quality of life. Patients suffer from severe losses of motor, sensory and autonomic nervous system functions. Controlled immunomodulation therapy is the key goal to replace non-specific immunosuppression, which is still the state of the art intervention after SCI today. Pro-inflammatory M1 macrophages are crucial players in the inflammatory response following SCI. These cells dominate the spinal cord after injury where they exert detrimental effects by secreting pro-inflammatory factors, by stimulating the formation of the inhibitory fibrotic scar and by attacking dystrophic axons. Collectively, this will negatively affect functional recovery of the patient. Therapies to improve functional outcome after SCI by suppressing the detrimental M1 macrophages via pro-regenerative M2 macrophages are a hot topic in the field of central nervous system repair. Surprisingly, the precise mechanisms by which M2 macrophages exert beneficial effects after SCI remain unknown. Therefore, this project aims to elucidate a new mechanism by which M2 macrophages suppress the M1 group and thereby improve functional recovery after SCI. By doing so, this project can identify new targets within this pathway which can be used for the development of clinically relevant strategies.
Date:1 Oct 2017 → 30 Sep 2021
Keywords:SPINAL CORD INJURY