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 language | English (US) |
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Pages (from-to) | 585-592 |
Number of pages | 8 |
Journal | Pain |
Volume | 153 |
Issue number | 3 |
DOIs | |
State | Published - Mar 2012 |
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Keywords
- Allodynia
- Galectin-3
- Herpes zoster
- Macrophage
- Microglia
- Spinal cord
ASJC Scopus subject areas
- Clinical Neurology
- Anesthesiology and Pain Medicine
- Neurology
- Pharmacology
Cite this
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 journal › Article
}
TY - JOUR
T1 - Contribution of spinal galectin-3 to acute herpetic allodynia in mice
AU - Takasaki, Ichiro
AU - Taniguchi, Kana
AU - Komatsu, Fumiaki
AU - Sasaki, Atsushi
AU - Andoh, Tsugunobu
AU - Nojima, Hiroshi
AU - Shiraki, Kimiyasu
AU - Hsu, Daniel K.
AU - Liu, Fu-Tong
AU - Kato, Ichiro
AU - Hiraga, Koichi
AU - Kuraishi, Yasushi
PY - 2012/3
Y1 - 2012/3
N2 - 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.
AB - 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.
KW - Allodynia
KW - Galectin-3
KW - Herpes zoster
KW - Macrophage
KW - Microglia
KW - Spinal cord
UR - http://www.scopus.com/inward/record.url?scp=84857359963&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84857359963&partnerID=8YFLogxK
U2 - 10.1016/j.pain.2011.11.022
DO - 10.1016/j.pain.2011.11.022
M3 - Article
C2 - 22197693
AN - SCOPUS:84857359963
VL - 153
SP - 585
EP - 592
JO - Pain
JF - Pain
SN - 0304-3959
IS - 3
ER -