ArticleThe Journal of allergy and clinical immunology2011
Functional KCa3.1 K+ channels are required for human fibrocyte migration.
Article in The Journal of allergy and clinical immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- KCa3.1 Inhibition Abrogates Suppression of Cell Migration and F-Actin Assembly Caused by Selective PIEZO1 Activation in Transformed Mouse Fibroblasts.International journal of molecular sciences · 2026Article
- The role and mechanism of vascular wall cell ion channels in vascular fibrosis remodeling.Channels (Austin, Tex.) · 2024Review
- CaBritish journal of pharmacology · 2020Review
- Ion Channels Orchestrate Pancreatic Ductal Adenocarcinoma Progression and Therapy.Frontiers in pharmacology · 2020Review
- KJournal of the American Heart Association · 2019Article
- Increased β2-adrenoceptor phosphorylation in airway smooth muscle in severe asthma: possible role of mast cell-derived growth factors.Clinical and experimental immunology · 2018Article
- Multi-walled carbon nanotubes act as a chemokine and recruit macrophages by activating the PLC/IP3/CRAC channel signaling pathway.Scientific reports · 2017Article
- Exon skipping of FcεRIβ eliminates expression of the high-affinity IgE receptor in mast cells with therapeutic potential for allergy.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The calcium-activated potassium channel KCa3.1 is an important modulator of hepatic injury.Scientific reports · 2016Article
- X-ray irradiation activates K+ channels via H2O2 signaling.Scientific reports · 2015Article
- Complementary roles of KCa3.1 channels and β1-integrin during alveolar epithelial repair.Respiratory research · 2015Article
- Orai/CRACM1 and KCa3.1 ion channels interact in the human lung mast cell plasma membrane.Cell communication and signaling : CCS · 2015Article
- The CD20 homologue MS4A4 directs trafficking of KIT toward clathrin-independent endocytosis pathways and thus regulates receptor signaling and recycling.Molecular biology of the cell · 2015Article
- Article
- Hydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease?Oxidative medicine and cellular longevity · 2015Review
- Increased constitutive αSMA and Smad2/3 expression in idiopathic pulmonary fibrosis myofibroblasts is KCa3.1-dependent.Respiratory research · 2014Article
- Functional KCa3.1 channels regulate steroid insensitivity in bronchial smooth muscle cells.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Circulating fibrocytes prepare the lung for cancer metastasis by recruiting Ly-6C+ monocytes via CCL2.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Ca(2+)-activated K(+) channel-3.1 blocker TRAM-34 attenuates airway remodeling and eosinophilia in a murine asthma model.American journal of respiratory cell and molecular biology · 2013Article
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundFibrocytes are bone marrow-derived CD34(+) collagen I-positive cells present in peripheral blood that develop α-smooth muscle actin expression and contractile activity in tissue culture. They are implicated in the pathogenesis of tissue remodeling and fibrosis in both patients with asthma and those with idiopathic pulmonary fibrosis. Targeting fibrocyte migration might therefore offer a new approach for the treatment of these diseases. Ion channels play key roles in cell function, but the ion-channel repertoire of human fibrocytes is unknown.
objectiveWe sought to examine whether human fibrocytes express the K(Ca)3.1 K(+) channel and to determine its role in cell differentiation, survival, and migration.
methodsFibrocytes were cultured from the peripheral blood of healthy subjects and patients with asthma. Whole-cell patch-clamp electrophysiology was used for the measurement of ion currents, whereas mRNA and protein were examined to confirm channel expression. Fibrocyte migration and proliferation assays were performed in the presence of K(Ca)3.1 ion-channel blockers.
resultsHuman fibrocytes cultured from the peripheral blood of both healthy control subjects and asthmatic patients expressed robust K(Ca)3.1 ion currents together with K(Ca)3.1 mRNA and protein. Two specific and distinct K(Ca)3.1 blockers (TRAM-34 and ICA-17043) markedly inhibited fibrocyte migration in transwell migration assays. Channel blockers had no effect on fibrocyte growth, apoptosis, or differentiation in cell culture.
conclusionsThe K(+) channel K(Ca)3.1 plays a key role in human fibrocyte migration. Currently available K(Ca)3.1-channel blockers might therefore attenuate tissue fibrosis and remodeling in patients with diseases such as idiopathic pulmonary fibrosis and asthma through the inhibition of fibrocyte recruitment.
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