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Table 2 sEVs in pain mechanisms

From: Current aspects of small extracellular vesicles in pain process and relief

Published year

Condition

sEV type

Mechanisms

Effects

Ref.

2022

Carrageenan-induced pain

CD200R+ macrophage-derived sEVs

CD200R+ sEVs transferred mitochondria to neurons in DRG

Resolved transient inflammatory pain

[21]

2021

CIBP

Cancer cell-derivd sEVs

Increased let-7d-5p in sEVs inhibited OPRM1 in DRG

Induced bone pain

[111]

2017,

2021

DRG neuron culture

NDEVs

TRPV1 activation promoted the release of miR-21-5p and miR-23a in NDEVs

Activated M1 macrophages

[53, 54]

2020

SNI

Serum-derived sEVs

Increased serum sEVs contained C5a and ICAM-1

/

[101]

2020

Metastatic cancer pain

Cancer cell-derivd sEVs

Increased gene expressions in sEVs

Induced mechanical allodynia and thermal hyperalgesia

[106]

2017

Lumbar disc herniation

NPs

Increased miR-223 in NPEVs at the acute phase

Attenuated the neuronal activity in the pain pathways

[114]

2017

CFA

Endosomes

Activated NK1R and CLR on endosomes

Promoted pain transmission

[121, 122]

2016

SNL

MDEVs

Increased MDEV-IL-1β in CSF and spinal cord

Reduced PWT and PWL

[59]

  1. NDEV Neuron-derived extracellular vesicle, SNI Spared nerve injury, SNL Spinal nerve ligation, MDEV Microglial-derived extracellular vesicles, DRG Dorsal root ganglion, PWT Paw withdrawal threshold, PWL Paw withdrawal latency, CIBP Cancer-induced bone pain, NP Nucleus pulposus, CFA Complete Freund’s adjuvant, TRPV-1 Transient receptor potential vanilloid 1, CLR Calcitonin receptor-like receptorsm NK1R Neurokinin 1 receptor, OPRM1 µ1 opioid receptor, DRG Dorsal root ganglion