ArticleExperimental and molecular pathology2011
C5b-9-activated, K(v)1.3 channels mediate oligodendrocyte cell cycle activation and dedifferentiation.
Article in Experimental and molecular pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- The validity of animal models to explore the pathogenic role of the complement system in multiple sclerosis: A review.Frontiers in molecular neuroscience · 2022Review
- IL-17 Inhibits Oligodendrocyte Progenitor Cell Proliferation and Differentiation by Increasing KFrontiers in cellular neuroscience · 2021Article
- Histone Deacetylase SIRT1 Mediates C5b-9-Induced Cell Cycle in Oligodendrocytes.Frontiers in immunology · 2020Article
- Kv1.3 Channel as a Key Therapeutic Target for Neuroinflammatory Diseases: State of the Art and Beyond.Frontiers in neuroscience · 2019Review
- Caveolin-1 facilitated KCNA5 expression, promoting breast cancer viability.Oncology letters · 2018Article
- A Kv1.3 channel-specific blocker alleviates neurological impairment through inhibiting T-cell activation in experimental autoimmune encephalomyelitis.CNS neuroscience & therapeutics · 2018Article
- Oligodendrocytes control potassium accumulation in white matter and seizure susceptibility.eLife · 2018Article
- The complement system as a biomarker of disease activity and response to treatment in multiple sclerosis.Immunologic research · 2017Review
- The Role of the Oligodendrocyte Lineage in Acute Brain Trauma.Neurochemical research · 2017Review
- Human immunodeficiency virus protein Tat induces oligodendrocyte injury by enhancing outward KNeurobiology of disease · 2017Article
- Regulation of Proliferation by a Mitochondrial Potassium Channel in Pancreatic Ductal Adenocarcinoma Cells.Frontiers in oncology · 2017Article
- Oligodendrocyte Injury and Pathogenesis of HIV-1-Associated Neurocognitive Disorders.Brain sciences · 2016Review
- Unconventional EGF-induced ERK1/2-mediated Kv1.3 endocytosis.Cellular and molecular life sciences : CMLS · 2016Article
- Activation of endogenously expressed ion channels by active complement in the retinal pigment epithelium.Pflugers Archiv : European journal of physiology · 2015Article
- Neuron-NG2 cell synapses: novel functions for regulating NG2 cell proliferation and differentiation.BioMed research international · 2013Review
- Membrane attack by complement: the assembly and biology of terminal complement complexes.Immunologic research · 2011Review
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14 authors at 2 institutions in 1 country.
Funding
Abstract
Voltage-gated potassium (K(v)) channels play an important role in the regulation of growth factor-induced cell proliferation. We have previously shown that cell cycle activation is induced in oligodendrocytes (OLGs) by complement C5b-9, but the role of K(v) channels in these cells had not been investigated. Differentiated OLGs were found to express K(v)1.4 channels, but little K(v)1.3. Exposure of OLGs to C5b-9 modulated K(v)1.3 functional channels and increased protein expression, whereas C5b6 had no effect. Pretreatment with the recombinant scorpion toxin rOsK-1, a highly selective K(v)1.3 inhibitor, blocked the expression of K(v)1.3 induced by C5b-9. rOsK-1 inhibited Akt phosphorylation and activation by C5b-9 but had no effect on ERK1 activation. These data strongly suggest a role for K(v)1.3 in controlling the Akt activation induced by C5b-9. Since Akt plays a major role in C5b-9-induced cell cycle activation, we also investigated the effect of inhibiting K(v)1.3 channels on DNA synthesis. rOsK-1 significantly inhibited the DNA synthesis induced by C5b-9 in OLG, indicating that K(v)1.3 plays an important role in the C5b-9-induced cell cycle. In addition, C5b-9-mediated myelin basic protein and proteolipid protein mRNA decay was completely abrogated by inhibition of K(v)1.3 expression. In the brains of multiple sclerosis patients, C5b-9 co-localized with NG2(+) OLG progenitor cells that expressed K(v)1.3 channels. Taken together, these data suggest that K(v)1.3 channels play an important role in controlling C5b-9-induced cell cycle activation and OLG dedifferentiation, both in vitro and in vivo.
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