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CD36 participates in PrP(106-126)-induced activation of microglia
Mohammed Kouadir1, Lifeng Yang, Rongrong Tan
1National Animal Transmissible Spongiform Encephalopathy Laboratory, College of Veterinary Medicine, China Agricultural University, Beijing, China.
Abstract:
Microglial activation is a characteristic feature of the pathogenesis of prion diseases. The molecular mechanisms that underlie prion-induced microglial activation are not very well understood. In the present study, we investigated the role of the class B scavenger receptor CD36 in microglial activation induced by neurotoxic prion protein (PrP) fragment 106-126 (PrP(106-126)). We first examined the time course of CD36 mRNA expression upon exposure to PrP(106-126) in BV2 microglia. We then analyzed different parameters of microglial activation in PrP(106-126)-treated cells in the presence or not of anti-CD36 monoclonal antibody (mAb). The cells were first incubated for 1 h with CD36 monoclonal antibody to block the CD36 receptor, and were then treated with neurotoxic prion peptides PrP(106-126). The results showed that PrP(106-126) treatment led to a rapid yet transitory increase in the mRNA expression of CD36, upregulated mRNA and protein levels of proinflammatory cytokines (IL-1β, IL-6 and TNF-α), increased iNOS expression and nitric oxide (NO) production, stimulated the activation of NF-κB and caspase-1, and elevated Fyn activity. The blockade of CD36 had no effect on PrP(106-126)-stimulated NF-κB activation and TNF-α protein release, abrogated the PrP(106-126)-induced iNOS stimulation, downregulated IL-1β and IL-6 expression at both mRNA and protein levels as well as TNF-α mRNA expression, decreased NO production and Fyn phosphorylation, reduced caspase-1 cleavage induced by moderate PrP(106-126)-treatment, but had no effect on caspase-1 activation after treatment with a high concentration of PrP(106-126). Together, these results suggest that CD36 is involved in PrP(106-126)-induced microglial activation and that the participation of CD36 in the interaction between PrP(106-126) and microglia may be mediated by Src tyrosine kinases. Our findings provide new insights into the mechanisms underlying the activation of microglia by neurotoxic prion peptides and open perspectives for new therapeutic strategies for prion diseases by modulation of CD36 signaling.
Insights
The scavenger receptor CD36 plays a role in prion disease pathogenesis by mediating microglial activation. Blocking CD36 reduces prion-induced inflammation and nitric oxide production, suggesting therapeutic potential.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Microglial activation is central to prion disease pathogenesis.
- The precise mechanisms of prion-induced microglial activation remain unclear.
- The role of scavenger receptors, like CD36, in this process is under investigation.
Purpose of the Study:
- To investigate the role of the class B scavenger receptor CD36 in microglial activation induced by a neurotoxic prion protein fragment (PrP(106-126)).
- To elucidate the molecular pathways involved in CD36-mediated microglial responses to prion peptides.
Main Methods:
- Examined CD36 mRNA expression in BV2 microglia exposed to PrP(106-126).
- Analyzed microglial activation parameters (cytokine expression, nitric oxide production, NF-κB and caspase-1 activation, Fyn activity) with and without anti-CD36 monoclonal antibody (mAb) blockade.
- Assessed the impact of CD36 blockade on PrP(106-126)-induced cellular responses.
Main Results:
- PrP(106-126) rapidly increased CD36 mRNA expression and upregulated pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), iNOS, nitric oxide, NF-κB, caspase-1, and Fyn activity.
- CD36 blockade abrogated PrP(106-126)-induced iNOS stimulation and decreased NO production, IL-1β, IL-6, TNF-α mRNA, and Fyn phosphorylation.
- CD36 blockade partially reduced caspase-1 cleavage and did not affect NF-κB activation or TNF-α protein release.
Conclusions:
- CD36 is implicated in PrP(106-126)-induced microglial activation.
- CD36's role in this interaction may involve Src tyrosine kinases.
- Findings offer insights into prion disease mechanisms and suggest CD36 modulation as a therapeutic strategy.
