Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/29163
Title: The C-terminus of murine S100A9 protein inhibits hyperalgesia induced by the agonist peptide of protease-activated receptor 2 (PAR(2))
Authors: Dale, C. S.
Cenac, N.
Britto, L. R. G.
Juliano, Maria Aparecida [UNIFESP]
Juliano, Luiz [UNIFESP]
Vergnolle, N.
Giorgi, R.
Univ Calgary
Butantan Inst
Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
Keywords: S100A9
antinociception
hyperalgesia
inflammation
PAR2
Egr-1
DRG neurons
HEK cells
KNRK-PAR(2) cells
Issue Date: 1-Oct-2006
Publisher: Nature Publishing Group
Citation: British Journal of Pharmacology. London: Nature Publishing Group, v. 149, n. 4, p. 374-384, 2006.
Abstract: Background and purpose: S100A9 protein induces anti-nociception in rodents, in different experimental models of inflammatory pain. Herein, we investigated the effects of a fragment of the C-terminus of S100A9 (mS100A9p), on the hyperalgesia induced by serine proteases, through the activation of protease-activated receptor-2 (PAR(2)).Experimental approach: Mechanical and thermal hyperalgesia induced by PAR(2) agonists (SLIGRL-NH2 and trypsin) was measured in rats submitted to the paw pressure or plantar tests, and Egr-1 expression was determined by immunohistochemistry in rat spinal cord dorsal horn. Calcium flux in human embryonic kidney cells (HEK), which naturally express PAR(2), in Kirsten virus-transformed kidney cells, transfected (KNRK-PAR(2)) or not (KNRK) with PAR(2), and in mouse dorsal root ganglia neurons (DRG) was measured by fluorimetric methods.Key results: mS100A9p inhibited mechanical hyperalgesia induced by trypsin, without modifying its enzymatic activity. Mechanical and thermal hyperalgesia induced by SLIGRL-NH2 were inhibited by mS100A9p. SLIGRL-NH2 enhanced Egr-1 expression, a marker of nociceptor activation, and this effect was inhibited by concomitant treatment with mS100A9p. mS100A9p inhibited calcium mobilization in DRG neurons in response to the PAR(2) agonists trypsin and SLIGRL-NH2, but also in response to capsaicin and bradykinin, suggesting a direct effect of mS100A9 on sensory neurons. No effect on the calcium flux induced by trypsin or SLIGRL in HEK cells or KNRK-PAR(2) cells was observed.Conclusions and implications: These data demonstrate that mS100A9p interferes with mechanisms involved in nociception and hyperalgesia and modulates, possibly directly on sensory neurons, the PAR(2)-induced nociceptive signal.
URI: http://repositorio.unifesp.br/handle/11600/29163
ISSN: 0007-1188
Other Identifiers: http://dx.doi.org/10.1038/sj.bjp.0706884
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