ArticleArthritis & rheumatology (Hoboken, N.J.)2015
KCa1.1 inhibition attenuates fibroblast-like synoviocyte invasiveness and ameliorates disease in rat models of rheumatoid arthritis.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Limosilactobacillus reuteri enables oral-to-systemic absorption of iberiotoxin for treatment of collagen-induced arthritis in rats.Microbial cell factories · 2025Article
- DLX4 regulates rheumatoid arthritis fibroblast-like synoviocytes invasiveness and a cancer transcriptomic signature.Scientific reports · 2025Article
- Exploring the therapeutic opportunities of potassium channels for the treatment of rheumatoid arthritis.Frontiers in pharmacology · 2024Review
- CaInternational journal of molecular sciences · 2023Review
- Article
- A bioengineered probiotic for the oral delivery of a peptide Kv1.3 channel blocker to treat rheumatoid arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Neuronal mechanism of a BK channelopathy in absence epilepsy and dyskinesia.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Antioxidant Carbon Nanoparticles Inhibit Fibroblast-Like Synoviocyte Invasiveness and Reduce Disease Severity in a Rat Model of Rheumatoid Arthritis.Antioxidants (Basel, Switzerland) · 2020Article
- Pro-inflammatory Cytokines Drive Deregulation of Potassium Channel Expression in Primary Synovial Fibroblasts.Frontiers in physiology · 2020Article
- An overview of carbonic anhydrases and membrane channels of synoviocytes in inflamed joints.Journal of enzyme inhibition and medicinal chemistry · 2019Review
- KCa1.1 and Kv1.3 channels regulate the interactions between fibroblast-like synoviocytes and T lymphocytes during rheumatoid arthritis.Arthritis research & therapy · 2019Article
- Targeting KCa1.1 Channels with a Scorpion Venom Peptide for the Therapy of Rat Models of Rheumatoid Arthritis.The Journal of pharmacology and experimental therapeutics · 2018Article
- Differences in ion channel phenotype and function between humans and animal models.Frontiers in bioscience (Landmark edition) · 2018Review
- KCa1.1 channels as therapeutic targets for rheumatoid arthritis.Expert opinion on therapeutic targets · 2017Article
- KCa1.1 channels regulate βFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Prolonged immunomodulation in inflammatory arthritis using the selective Kv1.3 channel blocker HsTX1[R14A] and its PEGylated analog.Clinical immunology (Orlando, Fla.) · 2017Article
- Pro-inflammatory CaScientific reports · 2017Article
- Detection of Matrix Metalloproteinases by Zymography.Methods in molecular biology (Clifton, N.J.) · 2017Article
- Functional KCa1.1 channels are crucial for regulating the proliferation, migration and differentiation of human primary skeletal myoblasts.Cell death & disease · 2016Article
- Different expression of β subunits of the KCa1.1 channel by invasive and non-invasive human fibroblast-like synoviocytes.Arthritis research & therapy · 2016Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveFibroblast-like synoviocytes (FLS) participate in joint inflammation and damage in rheumatoid arthritis (RA) and its animal models. The purpose of this study was to define the importance of KCa1.1 (BK, Maxi-K, Slo1, KCNMA1) channel expression and function in FLS and to establish these channels as potential new targets for RA therapy.
methodsWe compared KCa1.1 expression levels in FLS from rats with pristane-induced arthritis (PIA) and in FLS from healthy rats. We then used ex vivo functional assays combined with small interfering RNA-induced knockdown, overexpression, and functional modulation of KCa1.1 in PIA FLS. Finally, we determined the effectiveness of modulating KCa1.1 in 2 rat models of RA, moderate PIA and severe collagen-induced arthritis (CIA).
resultsWe found that PIA FLS expressed the KCa1.1 channel as their major potassium channel, as has been found in FLS from patients with RA. In contrast, FLS from healthy rats expressed fewer of these channels. Inhibiting the function or expression of KCa1.1 ex vivo reduced proliferation and invasive properties of, as well as protease production by, PIA FLS, whereas opening native KCa1.1 or overexpressing the channel enhanced the invasiveness of both FLS from rats with PIA and FLS from healthy rats. Treatment with a KCa1.1 channel blocker at the onset of clinical signs stopped disease progression in the PIA and CIA models, reduced joint and bone damage, and inhibited FLS invasiveness and proliferation.
conclusionOur results demonstrate a critical role of KCa1.1 channels in the regulation of FLS invasiveness and suggest that KCa1.1 channels represent potential therapeutic targets in RA.
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