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PURPOSE: Traumatic nerve injuries often result in loss of function despite optimal surgical management. One reason for poor recovery is the degradation of the neuromuscular junction(NMJ) after injury. Our lab has previously shown the novel finding that preservation of the NMJ after nerve injury actually improves functional recovery following reinnervation. Developmental neurobiology literature suggest that Agrin, a proteoglycan involved in synaptogenesis, may play a critical role in NMJ preservation. Our experiments with a murine model demonstrated that genetic deletion of MMP-3, a matrix-metalloproteinase that degrades agrin on a homeostatic basis, allowed sufficient agrin levels to remain in denervated motor endplates. Moreover, our lab further demonstrated that denervated motor endplates with sufficient agrin levels have superior morphometric qualities and are highly conducive to promoting successful reinnervation. Here, we sought to determine if direct local delivery of agrin after a traumatic nerve injury might preserve the motor endplates.

plastic and reconstructive surgery. global open

Abstract 57: Expression Of Markers For Pericytes And Myofibroblasts In Bleomycin-induced Dermal Fibrosis: Potential Role Of Neuropeptide Receptors In A Mouse Model For Scleroderma