Original Article

Spinal Cord (2008) 46, 364–371; doi:10.1038/sj.sc.3102148; published online 27 November 2007

TGF-bold beta1 and TGF-bold beta2 expression after traumatic human spinal cord injury

A Buss1, K Pech1, B A Kakulas2, D Martin3, J Schoenen4, J Noth1 and G A Brook1,5

  1. 1Department of Neurology, Aachen University Hospital, Rheinisch-Westfälische Technische Hochschule (RWTH) Aachen, Aachen, Germany
  2. 2Center for Neuromuscular and Neurological Disorders, University of Western Australia, Perth, Western Australia, Australia
  3. 3Department of Neurosurgery, Sart Tilman Hospital, University of Liège, Liège, Belgium
  4. 4Departments of Neurology and Neuroanatomy, University of Liège, Liège, Belgium
  5. 5Department of Neuropathology, Aachen University Hospital, Rheinisch-Westfälische Technische Hochschule (RWTH) Aachen, Aachen, Germany

Correspondence: Dr A Buss, Department of Neurology, Aachen University Hospital, Pauwelsstrasse 30, Aachen 52074, Germany. E-mail: abuss@ukaachen.de

Received 19 March 2007; Revised 13 September 2007; Accepted 18 October 2007; Published online 27 November 2007.

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Abstract

Study design:

 

Immunohistochemical investigation in control and lesioned human spinal cords.

Objectives:

 

To assess the spatial and temporal expression patterns of transforming growth factor-beta1 and -beta2 (TGF-beta1 and TGF-beta2) in the human spinal cord after traumatic injury.

Setting:

 

Germany, Aachen, Aachen University Hospital.

Methods:

 

Sections from human spinal cords from 4 control patients and from 14 patients who died at different time points after traumatic spinal cord injury (SCI) were investigated immunohistochemically.

Results:

 

In control cases, TGF-beta1 was confined to occasional blood vessels, intravascular monocytes and some motoneurons, whereas TGF-beta2 was only found in intravascular monocytes. After traumatic SCI, TGF-beta1 immunoreactivity was dramatically upregulated by 2 days after injury (the earliest survival time investigated) and was detected within neurons, astrocytes and invading macrophages. The staining was most intense over the first weeks after injury but gradually declined by 1 year. TGF-beta2 immunoreactivity was first detected 24 days after injury. It was located in macrophages and astrocytes and remained elevated for up to 1 year. In white matter tracts undergoing Wallerian degeneration, there was no induction of either isoform.

Conclusion:

 

The early induction of TGF-beta1 at the point of SCI suggests a role in the acute inflammatory response and formation of the glial scar, while the later induction of TGF-beta2 may indicate a role in the maintenance of the scar. Neither of these TGF-beta isoforms appears to contribute to the astrocytic scar formation in nerve fibre tracts undergoing Wallerian degeneration.

Keywords:

spinal cord injury, Wallerian degeneration, scar, inflammation

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