Journal
GLIA
Volume 70, Issue 1, Pages 71-88Publisher
WILEY
DOI: 10.1002/glia.24089
Keywords
cannabinoid receptor 2 (CB2); endocannabinoid system; microglia; neuroinflammation; RNA sequencing
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Funding
- ERA CVD [00160389]
- Else-Kroner-Fresenius Stiftung [2018_A158]
- BONFOR [O-178.0016]
- Germany's Excellence Strategy [EXC2151, 390873048]
- Deutsche Forschungsgemeinschaft (DFG, German Research Foundation)
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Tight regulation of microglial activity is crucial for precise responses to threats, as uncontrolled activity can be neurotoxic. Cannabinoid receptor 2 (CB2) signaling plays a key role in controlling microglial homeostasis and activation, impacting the response to Toll-like receptor (TLR) mediated activation. The deletion of CB2 leads to dampened transcriptional response and distinct gene expression profiles in microglia, influencing their activation programs.
The tight regulation of microglia activity is key for precise responses to potential threats, while uncontrolled and exacerbated microglial activity is neurotoxic. Microglial toll-like receptors (TLRs) are indispensable for sensing different types of assaults and triggering an innate immune response. Cannabinoid receptor 2 (CB2) signaling is a key pathway to control microglial homeostasis and activation, and its activation is connected to changes in microglial activity. We aimed to investigate how CB2 signaling impacts TLR-mediated microglial activation. Here, we demonstrate that deletion of CB2 causes a dampened transcriptional response to prototypic TLR ligands in microglia. Loss of CB2 results in distinct microglial gene expression profiles, morphology, and activation. We show that the CB2-mediated attenuation of TLR-induced microglial activation is mainly p38 MAPK-dependent. Taken together, we demonstrate that CB2 expression and signaling are necessary to fine-tune TLR-induced activation programs in microglia.
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