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Regulation of Wnt signaling by nociceptive input in animal models.

Shi Y, Yuan S, Li B, Wang J, Carlton SM, Chung K, Chung JM, Tang SJ - Mol Pain (2012)

Bottom Line: In addition, Wnt3a, a prototypic Wnt ligand that activates the canonical pathway, is also enriched in the superficial layers.Furthermore, Wnt5a, a prototypic Wnt ligand for non-canonical pathways, and its receptor Ror2 are also up-regulated in the SCDH of these models.Our results suggest that Wnt signaling pathways are regulated by nociceptive input.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX 77555, USA.

ABSTRACT

Background: Central sensitization-associated synaptic plasticity in the spinal cord dorsal horn (SCDH) critically contributes to the development of chronic pain, but understanding of the underlying molecular pathways is still incomplete. Emerging evidence suggests that Wnt signaling plays a crucial role in regulation of synaptic plasticity. Little is known about the potential function of the Wnt signaling cascades in chronic pain development.

Results: Fluorescent immunostaining results indicate that β-catenin, an essential protein in the canonical Wnt signaling pathway, is expressed in the superficial layers of the mouse SCDH with enrichment at synapses in lamina II. In addition, Wnt3a, a prototypic Wnt ligand that activates the canonical pathway, is also enriched in the superficial layers. Immunoblotting analysis indicates that both Wnt3a a β-catenin are up-regulated in the SCDH of various mouse pain models created by hind-paw injection of capsaicin, intrathecal (i.t.) injection of HIV-gp120 protein or spinal nerve ligation (SNL). Furthermore, Wnt5a, a prototypic Wnt ligand for non-canonical pathways, and its receptor Ror2 are also up-regulated in the SCDH of these models.

Conclusion: Our results suggest that Wnt signaling pathways are regulated by nociceptive input. The activation of Wnt signaling may regulate the expression of spinal central sensitization during the development of acute and chronic pain.

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Cellular localization of Wnt3a and Wnt5a in DRGs.A-C: Double-staining of Wnt3a (A) and NeuN (B). Wnt3a is mainly detected in NeuN-labeled cells in DRGs (C). D-F: Double-staining of Wnt5a (D) and NeuN (E). Wnt5a is largely detected in NeuN-labeled DRG neurons (F). Scale bar: 50 μm.
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Figure 5: Cellular localization of Wnt3a and Wnt5a in DRGs.A-C: Double-staining of Wnt3a (A) and NeuN (B). Wnt3a is mainly detected in NeuN-labeled cells in DRGs (C). D-F: Double-staining of Wnt5a (D) and NeuN (E). Wnt5a is largely detected in NeuN-labeled DRG neurons (F). Scale bar: 50 μm.

Mentions: We also determined the cellular localization of Wnt3a in DRGs. As shown in Figure 5 A-C, Wnt3a was expressed in NeuN-labeled neurons in DRGs (L4/L5 levels). Similarly, Wnt5a staining was also largely restricted to DRG neurons (Figure 5 D-F). Little Wnt3a or Wnt5a staining was detected in non-neuronal cells. Thus, Wnt3a and Wnt5a are expressed in neurons both in the spinal cord and the DRGs.


Regulation of Wnt signaling by nociceptive input in animal models.

Shi Y, Yuan S, Li B, Wang J, Carlton SM, Chung K, Chung JM, Tang SJ - Mol Pain (2012)

Cellular localization of Wnt3a and Wnt5a in DRGs.A-C: Double-staining of Wnt3a (A) and NeuN (B). Wnt3a is mainly detected in NeuN-labeled cells in DRGs (C). D-F: Double-staining of Wnt5a (D) and NeuN (E). Wnt5a is largely detected in NeuN-labeled DRG neurons (F). Scale bar: 50 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3472283&req=5

Figure 5: Cellular localization of Wnt3a and Wnt5a in DRGs.A-C: Double-staining of Wnt3a (A) and NeuN (B). Wnt3a is mainly detected in NeuN-labeled cells in DRGs (C). D-F: Double-staining of Wnt5a (D) and NeuN (E). Wnt5a is largely detected in NeuN-labeled DRG neurons (F). Scale bar: 50 μm.
Mentions: We also determined the cellular localization of Wnt3a in DRGs. As shown in Figure 5 A-C, Wnt3a was expressed in NeuN-labeled neurons in DRGs (L4/L5 levels). Similarly, Wnt5a staining was also largely restricted to DRG neurons (Figure 5 D-F). Little Wnt3a or Wnt5a staining was detected in non-neuronal cells. Thus, Wnt3a and Wnt5a are expressed in neurons both in the spinal cord and the DRGs.

Bottom Line: In addition, Wnt3a, a prototypic Wnt ligand that activates the canonical pathway, is also enriched in the superficial layers.Furthermore, Wnt5a, a prototypic Wnt ligand for non-canonical pathways, and its receptor Ror2 are also up-regulated in the SCDH of these models.Our results suggest that Wnt signaling pathways are regulated by nociceptive input.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX 77555, USA.

ABSTRACT

Background: Central sensitization-associated synaptic plasticity in the spinal cord dorsal horn (SCDH) critically contributes to the development of chronic pain, but understanding of the underlying molecular pathways is still incomplete. Emerging evidence suggests that Wnt signaling plays a crucial role in regulation of synaptic plasticity. Little is known about the potential function of the Wnt signaling cascades in chronic pain development.

Results: Fluorescent immunostaining results indicate that β-catenin, an essential protein in the canonical Wnt signaling pathway, is expressed in the superficial layers of the mouse SCDH with enrichment at synapses in lamina II. In addition, Wnt3a, a prototypic Wnt ligand that activates the canonical pathway, is also enriched in the superficial layers. Immunoblotting analysis indicates that both Wnt3a a β-catenin are up-regulated in the SCDH of various mouse pain models created by hind-paw injection of capsaicin, intrathecal (i.t.) injection of HIV-gp120 protein or spinal nerve ligation (SNL). Furthermore, Wnt5a, a prototypic Wnt ligand for non-canonical pathways, and its receptor Ror2 are also up-regulated in the SCDH of these models.

Conclusion: Our results suggest that Wnt signaling pathways are regulated by nociceptive input. The activation of Wnt signaling may regulate the expression of spinal central sensitization during the development of acute and chronic pain.

Show MeSH
Related in: MedlinePlus