DICAM in the Extracellular Vesicles from Astrocytes Attenuates Microglia Activation and Neuroinflammation

Cross-talk between astrocytes and microglia plays an important role in neuroinflammation and central sensitization, but the manner in which glial cells interact remains less well-understood. Herein, we investigated the role of dual immunoglobulin domain-containing cell adhesion molecules (DICAM) in...

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Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2022-09, Vol.11 (19), p.2977
Main Authors: Han, Jin, Cho, Hyun-Jung, Park, Donghwi, Han, Seungwoo
Format: Article
Language:English
Subjects:
Animals
astrocyte
Astrocytes
Astrocytes - metabolism
Care and treatment
Cell activation
Cell adhesion molecules
Cell Adhesion Molecules - metabolism
Cell organelles
Complex regional pain syndrome
CRPS
Cytokines
DICAM
extracellular vesicle
Extracellular vesicles
Extracellular Vesicles - metabolism
General anesthesia
Glial cells
Health aspects
Immobilization
Inflammation
MAP kinase
Mice
Mice, Knockout
Microglia
Microglia - metabolism
Nervous system diseases
neuroinflammation
Neuroinflammatory Diseases
Neuronal-glial interactions
p38 Mitogen-Activated Protein Kinases - metabolism
Pain
Pain perception
Proteins
Spinal cord
Tibia
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Summary:Cross-talk between astrocytes and microglia plays an important role in neuroinflammation and central sensitization, but the manner in which glial cells interact remains less well-understood. Herein, we investigated the role of dual immunoglobulin domain-containing cell adhesion molecules (DICAM) in the glial cell interaction during neuroinflammation. DICAM knockout (KO) mice revealed enhanced nociceptive behaviors and glial cell activation of the tibia fracture with a cast immobilization model of complex regional pain syndrome (CRPS). DICAM was selectively secreted in reactive astrocytes, mainly via extracellular vesicles (EVs), and contributed to the regulation of neuroinflammation through the M2 polarization of microglia, which is dependent on the suppression of p38 MAPK signaling. In conclusion, DICAM secreted from reactive astrocytes through EVs was involved in the suppression of microglia activation and subsequent attenuation of neuroinflammation during central sensitization.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells11192977