A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Elevated 18:0 lysophosphatidylcholine contributes to the development of pain in tissue injury
Tekijät: Friston Dominic Anthony, Cuddihy Joshua, Souza Luiz Jessica, Truong An Hoai, Ho Laptin, Basra Meirvaan, Santha Peter, Oszlacs Orsolya, de Sousa Valente Joao, Marczylo Tim, Junttila Sini, Laycock Helen, Collins Declan, Vizcaychipi Marcela, Gyenesei Attila, Takats Zoltan, Jancso Gabor, Want Elizabeth, Nagy Istvan
Kustantaja: LIPPINCOTT WILLIAMS & WILKINS
Julkaisuvuosi: 2023
Journal: PAIN
Tietokannassa oleva lehden nimi: PAIN
Lehden akronyymi: PAIN
Vuosikerta: 164
Numero: 2
Aloitussivu: E103
Lopetussivu: E115
Sivujen määrä: 13
ISSN: 0304-3959
DOI: https://doi.org/10.1097/j.pain.0000000000002709
Verkko-osoite: http://dx.doi.org/10.1097/j.pain.0000000000002709
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/178885079
Tissue injuries, including burns, are major causes of death and morbidity worldwide. These injuries result in the release of intracellular molecules and subsequent inflammatory reactions, changing the tissues' chemical milieu and leading to the development of persistent pain through activating pain-sensing primary sensory neurons. However, the majority of pain-inducing agents in injured tissues are unknown. Here, we report that, amongst other important metabolite changes, lysophosphatidylcholines (LPCs) including 18:0 LPC exhibit significant and consistent local burn injury-induced changes in concentration. 18:0 LPC induces immediate pain and the development of hypersensitivities to mechanical and heat stimuli through molecules including the transient receptor potential ion channel, vanilloid subfamily, member 1, and member 2 at least partly via increasing lateral pressure in the membrane. As levels of LPCs including 18:0 LPC increase in other tissue injuries, our data reveal a novel role for these lipids in injury-associated pain. These findings have high potential to improve patient care.
Ladattava julkaisu This is an electronic reprint of the original article. |