Our goal is to explore and promote neural regeneration after spinal cord injury or disease.
Regenerative capacity is unevenly distributed across organisms. While mammals exhibit limited abilities to repair spinal cord damage, adult zebrafish are capable of remarkable cellular and functional regeneration after complete spinal cord transection. We hypothesize that fundamental mechanisms of innate spinal cord repair are either dormant, inefficient, or overshadowed by anti-regenerative effects in mammals, and that our zebrafish research will help promote these mechanisms across species.
In zebrafish, specialized bridging glial cells connect the transected spinal cord and are thought to support axon regrowth across the lesion. We have pursued a number of approaches to elucidate glial bridging mechanisms in zebrafish.
- Elucidating cellular and molecular mechanisms of ctgfa-dependent glial bridging in zebrafish.
- Defining the molecular identity of bridging glial cells in zebrafish.
- Screening for glial bridging factors in zebrafish.
Adult zebrafish are capable of adult neurogenesis in response to injury.
- New regulators of neurogenesis and functional repair in zebrafish.
- Ependymal cell contribution to neurogenesis in the adult spinal cord.
- Comprehensive analysis of glial and non-glial cell fates using Single nuclear RNA sequencing.
- Screening for new regulators of spinal cord repair and functional regeneration in zebrafish.
- Comparative studies between zebrafish bridging glia and mammalian glial cells to uncover the bases for differential regenerative capacity between the highly regenerative zebrafish and poorly regenerative mouse models.
- Reprogramming human cells into zebrafish-like bridging glia to promote spinal cord repair.