Publication:
Proof-of concept that an acute trophic factors intervention after spinal cord injury provides an adequate niche for neuroprotection, recruitment of nestin-expressing progenitors and regeneration

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Issued Date

2016

Resource Type

Article

File Type

application/pdf

ISSN

3643190

DOI

10.1007/s11064-016-1850-z

Other identifier(s)

2-s2.0-84958751578

Rights Holder(s)

Scopus

Bibliographic Citation

Neurochemical Research. Vol 41, (2016), p.431-449

Suggested Citation

Krityakiarana W., Zhao P.M., Nguyen K., Gomez-Pinilla F., Kotchabhakdi N., De Vellis J., Espinosa-Jeffrey A. Proof-of concept that an acute trophic factors intervention after spinal cord injury provides an adequate niche for neuroprotection, recruitment of nestin-expressing progenitors and regeneration. Neurochemical Research. Vol 41, (2016), p.431-449. doi:10.1007/s11064-016-1850-z Retrieved from: https://hdl.handle.net/20.500.14740/5639

Title

Proof-of concept that an acute trophic factors intervention after spinal cord injury provides an adequate niche for neuroprotection, recruitment of nestin-expressing progenitors and regeneration

Author(s)

Krityakiarana W.
 Zhao P.M.
 Nguyen K.
 Gomez-Pinilla F.
 Kotchabhakdi N.
 De Vellis J.
 Espinosa-Jeffrey A.

Abstract

Trophic factor treatment has been shown to improve the recovery of brain and spinal cord injury (SCI). In this study, we examined the effects of TSC1 (a combination of insulin-like growth factor 1 and transferrin) 4 and 8 h after SCI at the thoracic segment level (T12) in nestin- GFP transgenic mice. TSC1 treatment for 4 and 8 h increased the number of nestin-expressing cells around the lesion site and prevented Wallerian degeneration. Treatment with TSC1 for 4 h significantly increased heat shock protein (HSP)-32 and HSP-70 expression 1 and 2 mm from lesion site (both, caudal and rostral). Conversely, the number of HSP-32 positive cells decreased after an 8-h TSC1 treatment, although it was still higher than in both, non-treated SCI and intact spinal cord animals. Furthermore, TSC1 increased NG2 expressing cell numbers and preserved most axons intact, facilitating remyelination and repair. These results support our hypothesis that TSC1 is an effective treatment for cell and tissue neuroprotection after SCI. An early intervention is crucial to prevent secondary damage of the injured SC and, in particular, to prevent Wallerian degeneration. © Springer Science+Business Media New York 2016.

Subject(s)

Brain derived neurotrophic factor
 Epidermal growth factor receptor
 Glial cell line derived neurotrophic factor
 Green fluorescent protein
 Heat shock protein 70
 Heme oxygenase 1
 Hybrid protein
 Intermediate filament protein
 Nestin
 Recombinant growth factor
 Somatomedin C
 Transferrin
 TSC1
 Unclassified drug
 Nestin
 Neuroprotective agent
 Animal cell
 Animal experiment
 Animal model
 Animal tissue
 Article
 Axon
 Cell count
 Cell regeneration
 Controlled study
 Cytoarchitecture
 Demyelination
 Early intervention
 Gray matter
 Immunohistochemistry
 Mitochondrion
 Motoneuron
 Mouse
 Neural stem cell
 Neuroprotection
 Nonhuman
 Oxidative stress
 Priority journal
 Protein expression
 Protein phosphorylation
 Remyelinization
 Spinal cord
 Spinal cord injury
 Stem cell niche
 Wallerian degeneration
 White matter
 Animal
 Metabolism
 Pathophysiology
 Spinal cord injury
 Stem cell
 Transgenic mouse
 Animals
 Mice
 Mice, Transgenic
 Nestin
 Neuroprotective Agents
 Spinal Cord Injuries
 Stem Cells

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URI

https://hdl.handle.net/20.500.14740/5639

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Scopus: Year 1983-2021

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