Heat shock protein 27

Developmental regulation and expression after peripheral nerve injury

Michael Costigan, Richard J. Mannion, Giles Kendall, Susan E. Lewis, Jason A. Campagna, Richard E. Coggeshall, Jacqueta Meridith-Middleton, Simon Tate, Clifford J. Woolf

Research output: Contribution to journalArticle

138 Citations (Scopus)

Abstract

The heat shock protein (HSP) 27 is constitutively expressed at low levels in medium-sized lumbar dorsal root ganglion (DRG) cells in adult rats. Transection of the sciatic nerve results in a nine/old upregulation of HSP27 mRNA and protein in axotomized neurons in the/psilateral DRG at 48 hr, without equivalent changes n the mRNAs encoding HSP56, HSP60, HSP70, and HSP90. Dorsal rhizotomy, injuring the central axon of the DRG neuron, does not upregulate HSP27 mRNA levels. After peripheral axotomy, HSP27 mRNA and protein are present in small, medium, and large DRG neurons, and HSP27 protein is transported anterogradely, accumulating in the dorsal horn and dorsal columns of the spinal cord, where it persists for several months. Axotomized motor neurons also upregulate HSP27. Only a minority of cultured adult DRG neurons are HSP27-immunoreactive soon after dissociation, but all express HSP27 after 24 hr in culture with prominent label throughout the neuron, including the growth cone. HSP27 differs from most axonal injury- regulated and growth-associated genes, which are typically present at high levels in early development and down-regulated on innerration of their targets, in that its mRNA is first detectable in the DRG late in development and only approaches adult levels by postnatal day 21. In non-neuronal cells, HSP27 has been shown to be involved both in actin filament dynamics and in protection against necrotic and apoptotic cell death. Therefore, its upregulation after adult peripheral nerve injury may both promote survival of the injured neurons and contribute to alterations in the cytoskeleton associated with axonal growth.

Original languageEnglish (US)
Pages (from-to)5891-5900
Number of pages10
JournalJournal of Neuroscience
Volume18
Issue number15
StatePublished - Aug 1 1998

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HSP27 Heat-Shock Proteins
Peripheral Nerve Injuries
Spinal Ganglia
Neurons
Up-Regulation
Messenger RNA
Rhizotomy
Axotomy
Growth Cones
Motor Neurons
Sciatic Nerve
Growth
Cytoskeleton
Actin Cytoskeleton
Axons
Spinal Cord
Cell Death
Wounds and Injuries
Genes

Keywords

  • Apoptosis
  • Axotomy
  • Differential gene expression
  • Dorsal root ganglion
  • Regeneration
  • Spinal cord

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Costigan, M., Mannion, R. J., Kendall, G., Lewis, S. E., Campagna, J. A., Coggeshall, R. E., ... Woolf, C. J. (1998). Heat shock protein 27: Developmental regulation and expression after peripheral nerve injury. Journal of Neuroscience, 18(15), 5891-5900.

Heat shock protein 27 : Developmental regulation and expression after peripheral nerve injury. / Costigan, Michael; Mannion, Richard J.; Kendall, Giles; Lewis, Susan E.; Campagna, Jason A.; Coggeshall, Richard E.; Meridith-Middleton, Jacqueta; Tate, Simon; Woolf, Clifford J.

In: Journal of Neuroscience, Vol. 18, No. 15, 01.08.1998, p. 5891-5900.

Research output: Contribution to journalArticle

Costigan, M, Mannion, RJ, Kendall, G, Lewis, SE, Campagna, JA, Coggeshall, RE, Meridith-Middleton, J, Tate, S & Woolf, CJ 1998, 'Heat shock protein 27: Developmental regulation and expression after peripheral nerve injury', Journal of Neuroscience, vol. 18, no. 15, pp. 5891-5900.
Costigan M, Mannion RJ, Kendall G, Lewis SE, Campagna JA, Coggeshall RE et al. Heat shock protein 27: Developmental regulation and expression after peripheral nerve injury. Journal of Neuroscience. 1998 Aug 1;18(15):5891-5900.
Costigan, Michael ; Mannion, Richard J. ; Kendall, Giles ; Lewis, Susan E. ; Campagna, Jason A. ; Coggeshall, Richard E. ; Meridith-Middleton, Jacqueta ; Tate, Simon ; Woolf, Clifford J. / Heat shock protein 27 : Developmental regulation and expression after peripheral nerve injury. In: Journal of Neuroscience. 1998 ; Vol. 18, No. 15. pp. 5891-5900.
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