A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä

Elevated 18:0 lysophosphatidylcholine contributes to the development of pain in tissue injury




TekijätFriston 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

KustantajaLIPPINCOTT WILLIAMS & WILKINS

Julkaisuvuosi2023

JournalPAIN

Tietokannassa oleva lehden nimiPAIN

Lehden akronyymiPAIN

Vuosikerta164

Numero2

AloitussivuE103

LopetussivuE115

Sivujen määrä13

ISSN0304-3959

DOIhttps://doi.org/10.1097/j.pain.0000000000002709

Verkko-osoitehttp://dx.doi.org/10.1097/j.pain.0000000000002709

Rinnakkaistallenteen osoitehttps://research.utu.fi/converis/portal/detail/Publication/178885079


Tiivistelmä
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.

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Last updated on 2024-26-11 at 20:43