ArticleApoptosis : an international journal on programmed cell death2014
The MEK/ERK pathway is the primary conduit for Borrelia burgdorferi-induced inflammation and P53-mediated apoptosis in oligodendrocytes.
Article in Apoptosis : an international journal on programmed cell death, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Diabetic peripheral neuropathy based on Schwann cell injury: mechanisms of cell death regulation and therapeutic perspectives.Frontiers in endocrinology · 2024Review
- Identifying platelet-derived factors as amplifiers of B. burgdorferi-induced cytokine production.Clinical and experimental immunology · 2022Article
- Intestinal alkaline phosphatase (IAP, IAP Enhancer) attenuates intestinal inflammation and alleviates insulin resistance.Frontiers in immunology · 2022Article
- Activation of Galanin Receptor 1 with M617 Attenuates Neuronal Apoptosis via ERK/GSK-3β/TIP60 Pathway After Subarachnoid Hemorrhage in Rats.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Lyme Neuroborreliosis: Mechanisms ofBrain sciences · 2021Review
- Ginkgolide B promotes oligodendrocyte precursor cell differentiation and survival via Akt/CREB/bcl-2 signaling pathway after white matter lesion.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Confirmed cases of Neuroborreliosis with involvement of peripheral nervous system: Description of a cohort.Medicine · 2020Observational
- Reappraisal of Human HOG and MO3.13 Cell Lines as a Model to Study Oligodendrocyte Functioning.Cells · 2019Article
- Cytokine Expression Patterns and Single Nucleotide Polymorphisms (SNPs) in Patients with Chronic Borreliosis.Antibiotics (Basel, Switzerland) · 2019Article
- Rhesus Brain Transcriptomic Landscape in anFrontiers in neuroscience · 2019Article
- Geniposide Attenuates LPS-Induced Injury via Up-Regulation of miR-145 in H9c2 Cells.Inflammation · 2018Article
- Intracellular TLR7 is activated in human oligodendrocytes in response to Borrelia burgdorferi exposure.Neuroscience letters · 2018Article
- Primary Human Microglia Are Phagocytically Active and Respond toFrontiers in microbiology · 2018Article
- GM1 Induced the inflammatory response related to the Raf-1/MEK1/2/ERK1/2 pathway in co-culture of pig mesenchymal stem cells with RAW264.7.Animal cells and systems · 2018Article
- Receptor tyrosine kinases play a significant role in human oligodendrocyte inflammation and cell death associated with the Lyme disease bacterium Borrelia burgdorferi.Journal of neuroinflammation · 2017Article
- MicroRNA and mRNA Transcriptome Profiling in Primary Human Astrocytes Infected with Borrelia burgdorferi.PloS one · 2017Article
- Chrysin induces cell apoptosis in human uveal melanoma cells via intrinsic apoptosis.Oncology letters · 2016Article
- Effects of High Glucose on Cell Viability and Differentiation in Primary Cultured Schwann Cells: Potential Role of ERK Signaling Pathway.Neurochemical research · 2016Article
- The Putative Role of Viruses, Bacteria, and Chronic Fungal Biotoxin Exposure in the Genesis of Intractable Fatigue Accompanied by Cognitive and Physical Disability.Molecular neurobiology · 2016Review
- Antagonist of the neurokinin-1 receptor curbs neuroinflammation in ex vivo and in vitro models of Lyme neuroborreliosis.Journal of neuroinflammation · 2015Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
Lyme neuroborreliosis (LNB) affects both the central and peripheral nervous systems. In a rhesus macaque model of LNB we had previously shown that brains of rhesus macaques inoculated with Borrelia burgdorferi release inflammatory mediators, and undergo oligodendrocyte and neuronal cell death. In vitro analysis of this phenomenon indicated that while B. burgdorferi can induce inflammation and apoptosis of oligodendrocytes per se, microglia are required for neuronal apoptosis. We hypothesized that the inflammatory milieu elicited by the bacterium in microglia or oligodendrocytes contributes to the apoptosis of neurons and glial cells, respectively, and that downstream signaling events in NFkB and/or MAPK pathways play a role in these phenotypes. To test these hypotheses in oligodendrocytes, several pathway inhibitors were used to determine their effect on inflammation and apoptosis, as induced by B. burgdorferi. In a human oligodendrocyte cell line (MO3.13), inhibition of the ERK pathway in the presence of B. burgdorferi markedly reduced inflammation, followed by the JNK, p38 and NFkB pathway inhibition. In addition to eliciting inflammation, B. burgdorferi also increased total p53 protein levels, and suppression of the ERK pathway mitigated this effect. While inhibition of p53 had a minimal effect in reducing inflammation, suppression of the ERK pathway or p53 reduced apoptosis as measured by active caspase-3 activity and the TUNEL assay. A similar result was seen in primary human oligodendrocytes wherein suppression of ERK or p53 reduced apoptosis. It is possible that inflammation and apoptosis in oligodendrocytes are divergent arms of MAPK pathways, particularly the MEK/ERK pathway.
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