ArticleJournal of molecular neuroscience : MN2015
Toll-like receptor 2 deficiency shifts PrP106-126-induced microglial activation from a neurotoxic to a neuroprotective phenotype.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
- Distinctive Toll-like Receptors Gene Expression and Glial Response in Different Brain Regions of Natural Scrapie.International journal of molecular sciences · 2022Article
- ABCA7, a Genetic Risk Factor Associated with Alzheimer's Disease Risk in African Americans.Journal of Alzheimer's disease : JAD · 2022Review
- Biologic TNF-α inhibitors reduce microgliosis, neuronal loss, and tau phosphorylation in a transgenic mouse model of tauopathy.Journal of neuroinflammation · 2021Article
- Activation of GPR40 attenuates neuroinflammation and improves neurological function via PAK4/CREB/KDM6B pathway in an experimental GMH rat model.Journal of neuroinflammation · 2021Article
- Specific depletion of resident microglia in the early stage of stroke reduces cerebral ischemic damage.Journal of neuroinflammation · 2021Article
- Senescent accelerated prone 8 (SAMP8) mice as a model of age dependent neuroinflammation.Journal of neuroinflammation · 2021Article
- Substantia nigra Smad3 signaling deficiency: relevance to aging and Parkinson's disease and roles of microglia, proinflammatory factors, and MAPK.Journal of neuroinflammation · 2020Article
- Microglia in Prion Diseases: Angels or Demons?International journal of molecular sciences · 2020Review
- IL-22 hinders antiviral T cell responses and exacerbates ZIKV encephalitis in immunocompetent neonatal mice.Journal of neuroinflammation · 2020Article
- CX3CL1/CX3CR1 axis attenuates early brain injury via promoting the delivery of exosomal microRNA-124 from neuron to microglia after subarachnoid hemorrhage.Journal of neuroinflammation · 2020Article
- Farnesoid X receptor knockout protects brain against ischemic injury through reducing neuronal apoptosis in mice.Journal of neuroinflammation · 2020Article
- The impact of hyperpolarization-activated cyclic nucleotide-gated (HCN) and voltage-gated potassium KCNQ/Kv7 channels on primary microglia function.Journal of neuroinflammation · 2020Article
- Systemic microbial TLR2 agonists induce neurodegeneration in Alzheimer's disease mice.Journal of neuroinflammation · 2020Article
- Let's make microglia great again in neurodegenerative disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion diseases are fatal neurodegenerative diseases characterized by spongiform change, neuronal loss, and gliosis involving microglial activation in the central nervous system. Microglial activation is thought to play a key role in the pathogenesis of prion disease; however, the molecular mechanisms underlying prion-induced microglial activation are not well understood. The present study underlines the importance of toll-like receptor (TLR)-2 in mediating PrP106-126-induced microglial activation. We found that PrP106-126 induced expression of proinflammatory molecules and TLR2 in microglial cells; however, functional blocking antibodies against TLR2 suppressed PrP106-126-induced expression of proinflammatory molecules. PrP106-126-induced expression of proinflammatory molecules was also reduced in microglial cells isolated from TLR2-/- mice compared to those isolated from wild-type mice. Consistent with the importance of nuclear factor kappa B (NF-κB) mediating TLR functions, NF-κB inhibition also inhibited PrP106-126-induced expression of proinflammatory molecules. To better understand the effect of TLR2 deficiency on active microglial cells, we studied the expression of Arg1 and Mrc1 and anti-inflammatory cytokines, which indicated that TLR2 deficiency in microglial cells results in a shift from neurotoxic to neuroprotective phenotype. Taken together, our results indicate that the TLR2 signaling pathway mediates PrP106-126-induced microglial activation and potentially reveal new therapeutic strategies for prion diseases that modulate TLR2 signaling.
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