Contribution of spinal galectin-3 to acute herpetic allodynia in mice

Ichiro Takasaki, Kana Taniguchi, Fumiaki Komatsu, Atsushi Sasaki, Tsugunobu Andoh, Hiroshi Nojima, Kimiyasu Shiraki, Daniel K. Hsu, Fu-Tong Liu, Ichiro Kato, Koichi Hiraga, Yasushi Kuraishi

Research output: Contribution to journalArticle

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Abstract

To identify endogenous factors involved in herpetic pain, we performed genome-wide microarray analysis of the spinal cord of mice that suffered from herpetic allodynia induced by inoculation with herpes simplex virus type 1, which revealed marked induction of galectin-3, a β-galactoside-binding lectin. Therefore, we investigated the role of galectin-3 in herpetic allodynia. The expression levels of galectin-3 mRNA and protein were increased with a temporal pattern similar to that of herpetic allodynia. Galectin-3-expressing cells were mainly localized in the superficial dorsal horn, round in shape, and positive for the macrophage/microglia markers Iba-1 and F4/80. In the deep dorsal horn, there were Iba-1-positive cells with ramified and stout processes, which were negative for galectin-3. In the superficial dorsal horn, there were many CD3-positive T cells, but most of the galectin-3-expressing cells were negative for CD3. Galectin-3-expressing cells were negative for the neuronal marker NeuN and the astrocyte marker glial fibrillary acidic protein antibody. Deficiency in galectin-3 markedly reduced herpetic allodynia, without showing an effect on herpes zoster-like skin lesions. Intrathecal injection of galectin-3 produced mechanical allodynia in naive mice, and intrathecal injections of anti-galectin-3 antibodies significantly reduced herpetic allodynia. The present results suggest that galectin-3 in infiltrating macrophages and/or resident microglia in the spinal dorsal horn contributes to herpetic allodynia. Galectin-3 may be a new therapeutic target for the treatment of herpes zoster-associated pain.

Original languageEnglish (US)
Pages (from-to)585-592
Number of pages8
JournalPain
Volume153
Issue number3
DOIs
StatePublished - Mar 2012

Fingerprint

Galectin 3
Hyperalgesia
Spinal Injections
Herpes Zoster
Microglia
Macrophages
Pain
Galactosides
Antibodies
Glial Fibrillary Acidic Protein
Human Herpesvirus 1
Microarray Analysis
Lectins
Astrocytes
Spinal Cord

Keywords

  • Allodynia
  • Galectin-3
  • Herpes zoster
  • Macrophage
  • Microglia
  • Spinal cord

ASJC Scopus subject areas

  • Clinical Neurology
  • Anesthesiology and Pain Medicine
  • Neurology
  • Pharmacology

Cite this

Takasaki, I., Taniguchi, K., Komatsu, F., Sasaki, A., Andoh, T., Nojima, H., ... Kuraishi, Y. (2012). Contribution of spinal galectin-3 to acute herpetic allodynia in mice. Pain, 153(3), 585-592. https://doi.org/10.1016/j.pain.2011.11.022

Contribution of spinal galectin-3 to acute herpetic allodynia in mice. / Takasaki, Ichiro; Taniguchi, Kana; Komatsu, Fumiaki; Sasaki, Atsushi; Andoh, Tsugunobu; Nojima, Hiroshi; Shiraki, Kimiyasu; Hsu, Daniel K.; Liu, Fu-Tong; Kato, Ichiro; Hiraga, Koichi; Kuraishi, Yasushi.

In: Pain, Vol. 153, No. 3, 03.2012, p. 585-592.

Research output: Contribution to journalArticle

Takasaki, I, Taniguchi, K, Komatsu, F, Sasaki, A, Andoh, T, Nojima, H, Shiraki, K, Hsu, DK, Liu, F-T, Kato, I, Hiraga, K & Kuraishi, Y 2012, 'Contribution of spinal galectin-3 to acute herpetic allodynia in mice', Pain, vol. 153, no. 3, pp. 585-592. https://doi.org/10.1016/j.pain.2011.11.022
Takasaki I, Taniguchi K, Komatsu F, Sasaki A, Andoh T, Nojima H et al. Contribution of spinal galectin-3 to acute herpetic allodynia in mice. Pain. 2012 Mar;153(3):585-592. https://doi.org/10.1016/j.pain.2011.11.022
Takasaki, Ichiro ; Taniguchi, Kana ; Komatsu, Fumiaki ; Sasaki, Atsushi ; Andoh, Tsugunobu ; Nojima, Hiroshi ; Shiraki, Kimiyasu ; Hsu, Daniel K. ; Liu, Fu-Tong ; Kato, Ichiro ; Hiraga, Koichi ; Kuraishi, Yasushi. / Contribution of spinal galectin-3 to acute herpetic allodynia in mice. In: Pain. 2012 ; Vol. 153, No. 3. pp. 585-592.
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abstract = "To identify endogenous factors involved in herpetic pain, we performed genome-wide microarray analysis of the spinal cord of mice that suffered from herpetic allodynia induced by inoculation with herpes simplex virus type 1, which revealed marked induction of galectin-3, a β-galactoside-binding lectin. Therefore, we investigated the role of galectin-3 in herpetic allodynia. The expression levels of galectin-3 mRNA and protein were increased with a temporal pattern similar to that of herpetic allodynia. Galectin-3-expressing cells were mainly localized in the superficial dorsal horn, round in shape, and positive for the macrophage/microglia markers Iba-1 and F4/80. In the deep dorsal horn, there were Iba-1-positive cells with ramified and stout processes, which were negative for galectin-3. In the superficial dorsal horn, there were many CD3-positive T cells, but most of the galectin-3-expressing cells were negative for CD3. Galectin-3-expressing cells were negative for the neuronal marker NeuN and the astrocyte marker glial fibrillary acidic protein antibody. Deficiency in galectin-3 markedly reduced herpetic allodynia, without showing an effect on herpes zoster-like skin lesions. Intrathecal injection of galectin-3 produced mechanical allodynia in naive mice, and intrathecal injections of anti-galectin-3 antibodies significantly reduced herpetic allodynia. The present results suggest that galectin-3 in infiltrating macrophages and/or resident microglia in the spinal dorsal horn contributes to herpetic allodynia. Galectin-3 may be a new therapeutic target for the treatment of herpes zoster-associated pain.",
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