Macrophage/microglia-producing transient increase of platelet-activating factor is involved in neuropathic pain.
iScience
; 27(4): 109466, 2024 Apr 19.
Article
en En
| MEDLINE
| ID: mdl-38715939
ABSTRACT
Peripheral nerve injury (PNI) induces debilitating neuropathic pain symptoms, such as tactile allodynia. Accumulating evidence suggests that the expression levels of various transcripts and proteins are drastically changed after PNI. Recent lipidome analysis demonstrates increased levels of diverse lipids in chronic pain conditions. We show that PNI transiently increases platelet-activating factor (PAF) levels, a potent inflammatory phospholipid mediator, in the dorsal root ganglia (DRG) and spinal cord. We revealed that macrophage and microglia-specific PAF-producing enzyme LPLAT9/LPCAT2 knockout mice (Cx3cr1CreERT2;Lpcat2flox/flox) failed to develop mechanical allodynia and to increase PAF levels in the DRG and spinal cord after PNI. Moreover, we observed the suppression of PNI-induced PAF increase in the spinal cord of PAF receptor knockout mice, indicating a self-amplification loop of PAF production. In conclusion, macrophages and microglia enhance PAF production, contributing to PNI-induced neuropathic pain. Additionally, PAF-PAF receptor signaling is a potential target of neuropathic pain control.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Idioma:
En
Revista:
IScience
Año:
2024
Tipo del documento:
Article
País de afiliación:
Japón
Pais de publicación:
Estados Unidos