ArticleAmerican journal of respiratory cell and molecular biology2010
Functional role of canonical transient receptor potential 1 and canonical transient receptor potential 3 in normal and asthmatic airway smooth muscle cells.
Article in American journal of respiratory cell and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 54 citations in OpenAlex.
- Article
- Estrogenic Modulation of Ionic Channels, Pumps and Exchangers in Airway Smooth Muscle.International journal of molecular sciences · 2023Review
- Calcium released by osteoclastic resorption stimulates autocrine/paracrine activities in local osteogenic cells to promote coupled bone formation.American journal of physiology. Cell physiology · 2022Article
- Targeting Airway Smooth Muscle Hypertrophy in Asthma: An Approach Whose Time Has Come.Journal of asthma and allergy · 2021Review
- Maintenance of intracellular Ca2+ basal concentration in airway smooth muscle (Review).International journal of molecular medicine · 2018Review
- Cellular Na+ handling mechanisms involved in airway smooth muscle contraction (Review).International journal of molecular medicine · 2017Review
- Distinct Effects of CaInternational journal of biological sciences · 2017Article
- Targeting the γ-Aminobutyric Acid A Receptor α4 Subunit in Airway Smooth Muscle to Alleviate Bronchoconstriction.American journal of respiratory cell and molecular biology · 2016Article
- Canonical transient receptor potential 3 channels activate NF-κB to mediate allergic airway disease via PKC-α/IκB-α and calcineurin/IκB-β pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Inositol 1,4,5-trisphosphate activates TRPC3 channels to cause extracellular Ca2+ influx in airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Testosterone-induced relaxation involves L-type and store-operated Ca2+ channels blockade, and PGE 2 in guinea pig airway smooth muscle.Pflugers Archiv : European journal of physiology · 2015Article
- TRP Channels in Respiratory Pathophysiology: the Role of Oxidative, Chemical Irritant and Temperature Stimuli.Current neuropharmacology · 2015Review
- Calcineurin upregulates local Ca(2+) signaling through ryanodine receptor-1 in airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Channelopathies.Korean journal of pediatrics · 2014Review
- TRPC3 regulates release of brain-derived neurotrophic factor from human airway smooth muscle.Biochimica et biophysica acta · 2013Article
- Airway smooth muscle in airway reactivity and remodeling: what have we learned?American journal of physiology. Lung cellular and molecular physiology · 2013Review
- Airway smooth muscle STIM1 and Orai1 are upregulated in asthmatic mice and mediate PDGF-activated SOCE, CRAC currents, proliferation, and migration.Pflugers Archiv : European journal of physiology · 2012Article
- Ion channels in asthma.The Journal of biological chemistry · 2011Review
- Cholecystokinin facilitates neuronal excitability in the entorhinal cortex via activation of TRPC-like channels.Journal of neurophysiology · 2011Article
- Transient receptor potential channels as therapeutic targets.Nature reviews. Drug discovery · 2011Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Canonical transient receptor potential (TRPC)-encoded nonselective cation channels (NSCCs) are crucial for many cellular responses in a variety of cells; however, their molecular expression and functional roles in airway smooth muscle cells (ASMCs) remain obscure. The objective of this study was to determine whether TRPC1 and TRPC3 molecules could be important molecular constituents of native NSCCs controlling the resting membrane potential (Vm) and [Ca(2+)](i) in freshly isolated normal and ovalbumin (OVA)-sensitized/-challenged mouse ASMCs. Western blotting, RT-PCR, single-channel recording, whole-cell current-clamp recording, and a fluorescence imaging system were used to determine TRPC expression, NSCC activity, resting Vm, and resting [Ca(2+)](i). Specific individual TRPC antibodies and siRNAs were applied to test their functional roles. TRPC1 and TRPC3 proteins and mRNAs were expressed in freshly isolated ASM tissues. TRPC3 antibodies blocked the activity of NSCCs and hyperpolarized the resting Vm in ASMCs, whereas TRPC1 antibodies had no effect. TRPC3, but not TRPC1 gene silencing, largely diminished NSCC activity, hyperpolarized the resting Vm, lowered the resting [Ca(2+)](i), and inhibited methacholine-induced increase in [Ca(2+)](i). In OVA-sensitized/-challenged ASMCs, NSCC activity was greatly augmented, resting Vm was depolarized, and TRPC3 protein expression was increased. TRPC1 and TRPC3 antibodies blocked the increased activity of NSCCs and membrane depolarization in OVA-sensitized/-challenged cells. TRPC3 is an important molecular component of native NSCCs contributing to the resting Vm and [Ca(2+)](i) in normal ASMCs, as well as membrane depolarization and hyperresponsiveness in OVA-sensitized/-challenged cells, whereas TRPC1-encoded NSCCs are only activated in OVA-sensitized/-challenged airway myocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.