Purple and white patternPersistent pain results in suffering and poor quality of life. In addition, the lack of proper control of persistent pain may lead to the development of physical and mental disabilities, which further devastate the patient’s quality of life. The main goal of our research activities is to identify pivotal mechanisms in neuronal processing of information induced by various persistent painful conditions, which could be used to develop new pain killers. Hence, our activities will ultimately improve patients’ quality of life.

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BibTex format

@article{Torres-Perez:2017:10.1038/srep41221,
author = {Torres-Perez, JV and Santha, P and Varga, A and Szucs, P and Sousa-Valante, J and Gaal, B and Sivado, M and Andreou, A and Beattie, S and Nagy, B and Matesz, K and Arthur, JSC and Jancso, G and Nagy, I},
doi = {10.1038/srep41221},
journal = {Scientific Reports},
title = {Phosphorylated histone 3 at serine 10 identifies activated spinal neurons and contributes to the development of tissue injury-associated pain},
url = {http://dx.doi.org/10.1038/srep41221},
volume = {7},
year = {2017}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Transcriptional changes in superficial spinal dorsal horn neurons (SSDHN) are essential in the development and maintenance of prolonged pain. Epigenetic mechanisms including post-translational modifications in histones are pivotal in regulating transcription. Here, we report that phosphorylation of serine 10 (S10) in histone 3 (H3) specifically occurs in a group of rat SSDHN following the activation of nociceptive primary sensory neurons by burn injury, capsaicin application or sustained electrical activation of nociceptive primary sensory nerve fibres. In contrast, brief thermal or mechanical nociceptive stimuli, which fail to induce tissue injury or inflammation, do not produce the same effect. Blocking N-methyl-D-aspartate receptors or activation of extracellular signal-regulated kinases 1 and 2, or blocking or deleting the mitogen- and stress-activated kinases 1 and 2 (MSK1/2), which phosphorylate S10 in H3, inhibit up-regulation in phosphorylated S10 in H3 (p-S10H3) as well as fos transcription, a down-stream effect of p-S10H3. Deleting MSK1/2 also inhibits the development of carrageenan-induced inflammatory heat hyperalgesia in mice. We propose that p-S10H3 is a novel marker for nociceptive processing in SSDHN with high relevance to transcriptional changes and the development of prolonged pain.
AU  - Torres-Perez,JV
AU  - Santha,P
AU  - Varga,A
AU  - Szucs,P
AU  - Sousa-Valante,J
AU  - Gaal,B
AU  - Sivado,M
AU  - Andreou,A
AU  - Beattie,S
AU  - Nagy,B
AU  - Matesz,K
AU  - Arthur,JSC
AU  - Jancso,G
AU  - Nagy,I
DO  - 10.1038/srep41221
PY  - 2017///
SN  - 2045-2322
TI  - Phosphorylated histone 3 at serine 10 identifies activated spinal neurons and contributes to the development of tissue injury-associated pain
T2  - Scientific Reports
UR  - http://dx.doi.org/10.1038/srep41221
UR  - http://hdl.handle.net/10044/1/43234
VL  - 7
ER  -
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