Mar 31, 2017

Local delivery of thyroid hormone enhances oligodendrogenesis and myelination after spinal cord injury

Journal of Neural Engineering
Robert B ShultzYinghui Zhong


Traumatic spinal cord injury (SCI) causes apoptosis of myelin-forming oligodendrocytes (OLs) and demyelination of surviving axons, resulting in conduction failure. Remyelination of surviving denuded axons provides a promising therapeutic target for spinal cord repair. While cell transplantation has demonstrated efficacy in promoting remyelination and functional recovery, the lack of ideal cell sources presents a major obstacle to clinical application. The adult spinal cord contains oligodendrocyte precursor cells and multipotent neural stem/progenitor cells that have the capacity to differentiate into mature, myelinating OLs. However, endogenous oligodendrogenesis and remyelination processes are limited by the upregulation of remyelination-inhibitory molecules in the post-injury microenvironment. Multiple growth factors/molecules have been shown to promote OL differentiation and myelination. In this study we screened these therapeutics and found that 3, 3', 5-triiodothyronine (T3) is the most effective in promoting oligodendrogenesis and OL maturation in vitro. However, systemic administration of T3 to achieve therapeutic doses in the injured spinal cord is likely to induce hyperthyroidism, resulting in serious side effects. In...Continue Reading

Mentioned in this Paper

Post-Traumatic Myelopathy
MRNA Maturation
Myelin Sheath
Malignant Neoplasm of Spinal Cord
Biologic Development
Administration Procedure
Neoplasm of Uncertain or Unknown Behavior of Spinal Cord

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