The objective of this project is to develop potential approaches to the therapy of brain and spinal cord injury. One approach is to limit the production or increase the degradation of chondroitin sulfate proteoglycans (CSPGs). We have demonstrated that the enzyme arylsulfatase B, which cleaves the 4-sulfate group from chondroitin sulfate only at the non-reducing end, can dramatically increase neuronal growth on substrates of chondroitin sulfate. We are now conducting experiments in collaboration with Bioaxone to determine the efficacy of ARSB in animal models of brain and spinal cord injury. We are conducting studies to understand the changes in cell motility and ECM formation in fibroblasts derived from patients with mutations in chondroitin sulfotransferases leading to Ehlers-Danlos syndrome. We hope to develop techniques to restore normal function to these fibroblasts and perhaps extend these studies to animal models of disesase.
| Pearson, Craig S; Mencio, Caitlin P; Barber, Amanda C et al. (2018) Identification of a critical sulfation in chondroitin that inhibits axonal regeneration. Elife 7: |
| Janecke, Andreas R; Li, Ben; Boehm, Manfred et al. (2016) The phenotype of the musculocontractural type of Ehlers-Danlos syndrome due to CHST14 mutations. Am J Med Genet A 170A:103-15 |
| Yi, Jae-Hyuk; Katagiri, Yasuhiro; Yu, Panpan et al. (2014) Receptor protein tyrosine phosphatase ? binds to neurons in the adult mouse brain. Exp Neurol 255:12-8 |
| Geller, Herbert M (2013) Above the genome. Int J Dev Neurosci 31:351-2 |
| Yi, Jae-Hyuk; Katagiri, Yasuhiro; Susarla, Bala et al. (2012) Alterations in sulfated chondroitin glycosaminoglycans following controlled cortical impact injury in mice. J Comp Neurol 520:3295-313 |
