NGFR-mRNA expression in sciatic nerve: a sensitive indicator of early stages of axonopathy

Roberson, Mya L.; Toews, Arrel D.; Bouldin, Thomas W.; Weaver, James; Goines, Nelson D.; Morell, Pierre

doi:10.1016/0169-328x(94)00211-v

Cited by 29 publications

(20 citation statements)

References 26 publications

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“…Expression of P 0 by Schwann cells, as suggested by previous data (see, e.g., Toews et al, 1990), is down-regulated during demyelination (secondary to the tellurium-induced block in cholesterol biosynthesis) and is then up-regulated during remyelination. NGF-R expression is markedly up-regulated during demyelination secondary to alterations in axon-Schwann cell interactions associated with demyelination, but it declines to low, near-normal levels during the remyelinating period (for references and additional discussion, see Roberson et al, 1995;Toews et al, 1997a).…”

Section: Mcp-1 Mrna Expression During Tellurium-induced Primary Demyementioning

confidence: 97%

Monocyte chemoattractant protein 1 is responsible for macrophage recruitment following injury to sciatic nerve

1998

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Following injury to the peripheral nervous system, circulating monocytes/macrophages are recruited to the damaged tissue, where they play vital roles during both nerve degeneration and subsequent regeneration. Monocyte chemoattractant protein-1 (MCP-1), a member of the C-C or beta-chemokine family, is a powerful leukocyte recruitment/activation factor that is relatively specific for monocytes/macrophages. Because these are the predominant leukocyte type recruited by injured nerve, we hypothesized that upregulation of MCP-1 expression is involved in recruitment of these cells. Indeed, assay of steady-state levels of MCP-1 mRNA in rat sciatic nerve during tellurium-induced primary demyelination indicated up-regulation of this chemokine with a peak after 3 days of tellurium exposure, preceding the peak of accumulation of phagocytic macrophages (assayed as lysozyme mRNA levels) by 6 days. Increasing levels of MCP-1 mRNA expression, induced by increasing levels of tellurium exposure, resulted in corresponding increases in subsequent recruitment of macrophages. In situ hybridization suggested that MCP-1 mRNA was localized in Schwann cells. No expression of MIP-2, which is a C-X-C or alpha-chemokine that is specific for recruitment of neutrophils, was detected, consistent with the lack of recruitment of significant numbers of these cells. In addition, we also investigated the response seen following nerve transection (axonal degeneration and secondary demyelination with no subsequent regeneration) and nerve crush (degeneration followed by regeneration). In these latter two nerve injury models, there was also a marked, early up-regulation of MCP-1 mRNA, with a time course that is compatible with a role for this chemokine in macrophage recruitment. We conclude that MCP-1 is involved in recruiting monocytes/macrophages to injured peripheral nerve and that the specificity of leukocyte types recruited results from specificity of chemokine production.

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Section: Mcp-1 Mrna Expression During Tellurium-induced Primary Demyementioning

confidence: 97%

Monocyte chemoattractant protein 1 is responsible for macrophage recruitment following injury to sciatic nerve

1998

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“…The p75 receptor is rapidly upregulated by Schwann cells after nerve injury (Heumann et al, 1987a(Heumann et al, , 1987bTaniuchi et al, 1988;Toma et al, 1992;Robertson et al, 1995;You et al, 1996), and is associated with promoting Schwann cell migration (Anton et al, 1994) as well as apoptosis (Ferri and Bisby, 1999). The exact function of the non-neuronal expression of p75 remains to be determined.…”

Section: P75 As An Inhibitor Of Axonal Growthmentioning

confidence: 99%

The neurotrophin receptors, trkB and p75, differentially regulate motor axonal regeneration

2001

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Neurotrophic factors that support neuronal survival are implicated in axonal regeneration after injury. Specifically, a strong role for BDNF in motor axonal regeneration has been suggested based on its pattern of expression after injury, as well as the expression of its receptors, trkB and p75. Despite considerable in vitro evidence, which demonstrate specific and distinct physiological responses elicited following trkB and p75 activation, relatively little is known about the function of these receptors in vivo. To investigate the roles of the trkB and p75 receptors in motor axonal regeneration, we have used a tibial (TIB)- common peroneal (CP) cross suture paradigm in p75 homozygous (-/-) knockout mice, trkB heterozygous (+/-) knockout mice, as well as in their wild-type controls. Contralateral intact TIB motoneurons, and axotomized TIB motoneurons that regenerated their axons 10 mm into the CP distal nerve stump were identified by fluorescent retrograde tracers and counted in the T11-L1 spinal segments. Regeneration was evaluated 2, 3, 4, 6, and 8 weeks after nerve repair. Compared to wild-type animals, there are significantly fewer intact TIB motoneurons in p75 (-/-), but not trkB (+/-) mice. The number of motoneurons that regenerated their axons was significantly increased in the p75 (-/-) knockout mice, but significantly attenuated in the trkB (+/-) mice compared to wild-type controls. These results suggest that p75 is important for motoneuronal survival during development, but p75 expression after injury serves to inhibit motor axonal regeneration. In addition, full expression of trkB is critical for complete axonal regeneration to proceed.

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“…The low affinity NGF receptor (a 75 kDa glycoprotein, p75), is not expressed in mature Schwann cells but is upregulated after injury (Heumann et al, 1987a,b;Robertson et al, 1995;Taniuchi et al, 1988). The upregulation is observed in Schwann cells in the distal stump 36 h following nerve transection (Toma et al, 1992) and is a sensitive indicator of Schwann cell responsiveness to the injury (Kerkhoff et al, 1991;Robertson et al, 1995).…”

Section: Introductionmentioning

confidence: 96%

“…Following nerve injury, Schwann cells in the distal nerve stump proliferate and synthesize regeneration associated proteins, including cell adhesion molecules (CAMs), growth factors, and the low affinity nerve growth factor receptor, p75 (Acheson et al, 1991;Funakoshi et al, 1993;Heumann et al, 1987a,b;Raivich et al, 1987Raivich et al, , 1991Robertson et al, 1995;Taniuchi et al, 1986Taniuchi et al, , 1988Toma et al, 1990;Fu and Gordon, 1997).…”

Section: Introductionmentioning

confidence: 98%

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The expression of the low affinity nerve growth factor receptor in long-term denervated Schwann cells

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NGFR-mRNA expression in sciatic nerve: a sensitive indicator of early stages of axonopathy

Cited by 29 publications

References 26 publications

Monocyte chemoattractant protein 1 is responsible for macrophage recruitment following injury to sciatic nerve

Monocyte chemoattractant protein 1 is responsible for macrophage recruitment following injury to sciatic nerve

The neurotrophin receptors, trkB and p75, differentially regulate motor axonal regeneration

The expression of the low affinity nerve growth factor receptor in long-term denervated Schwann cells

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