ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010
Differential induction of CD38 expression by TNF-{alpha} in asthmatic airway smooth muscle cells.
Article in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- Integrative Roles of Pro-Inflammatory Cytokines on Airway Smooth Muscle Structure and Function in Asthma.Immunological reviews · 2025Review
- Bronchomotor tone imbalance evokes airway hyperresponsiveness.Expert review of respiratory medicine · 2024Review
- Mechanistic Links Between Obesity and Airway Pathobiology Inform Therapies for Obesity-Related Asthma.Paediatric drugs · 2023Review
- Airway smooth muscle in contractility and remodeling of asthma: potential drug target mechanisms.Expert opinion on therapeutic targets · 2023Article
- Airway smooth muscle and airway hyperresponsiveness in asthma: mechanisms of airway smooth muscle dysfunction.Minerva medica · 2022Article
- Novel Pathway of Adenosine Generation in the Lungs from NADMolecules (Basel, Switzerland) · 2020Article
- Role of CD38/cADPR signaling in obstructive pulmonary diseases.Current opinion in pharmacology · 2020Review
- DNA methyltransferase inhibitors upregulate CD38 protein expression and enhance daratumumab efficacy in multiple myeloma.Leukemia · 2020Article
- Airway Smooth Muscle-Specific Transcriptomic Signatures of Glucocorticoid Exposure.American journal of respiratory cell and molecular biology · 2019Article
- Salicylic acid amplifies Carbachol-induced bronchoconstriction in human precision-cut lung slices.Respiratory research · 2019Article
- Modulation of Bronchomotor Tone Pathways in Airway Smooth Muscle Function and Bronchomotor Tone in Asthma.Clinics in chest medicine · 2019Review
- Maintenance of intracellular Ca2+ basal concentration in airway smooth muscle (Review).International journal of molecular medicine · 2018Review
- CD38/cADPR Signaling Pathway in Airway Disease: Regulatory Mechanisms.Mediators of inflammation · 2018Review
- CD38 in the pathogenesis of allergic airway disease: Potential therapeutic targets.Pharmacology & therapeutics · 2017Review
- Formaldehyde Induces Rho-Associated Kinase Activity to Evoke Airway Hyperresponsiveness.American journal of respiratory cell and molecular biology · 2016Article
- Tumor Necrosis Factor Alpha Inhibits L-Type Ca(2+) Channels in Sensitized Guinea Pig Airway Smooth Muscle through ERK 1/2 Pathway.Mediators of inflammation · 2016Article
- Epigenetic targets for novel therapies of lung diseases.Pharmacology & therapeutics · 2015Review
- CD38 and airway hyper-responsiveness: studies on human airway smooth muscle cells and mouse models.Canadian journal of physiology and pharmacology · 2015Review
- MicroRNA-708 regulates CD38 expression through signaling pathways JNK MAP kinase and PTEN/AKT in human airway smooth muscle cells.Respiratory research · 2014Article
- Airway smooth muscle in airway reactivity and remodeling: what have we learned?American journal of physiology. Lung cellular and molecular physiology · 2013Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The ADP-ribosyl cyclase activity of CD38, a membrane protein expressed in human airway smooth muscle (ASM) cells, generates cyclic ADP-ribose (cADPR), a Ca²(+)-mobilizing agent. cADPR-mediated Ca²(+) responses to agonists are augmented in human ASM cells by TNF-α. CD38-deficient mice fail to develop airway hyperresponsiveness following intranasal TNF-α or IL-13 challenge, suggesting a role in asthma. The role of CD38 in human asthma remains unknown. We hypothesized that CD38 expression will be elevated in ASM cells from asthmatic donors (ASMA cells). CD38 mRNA and ADP-ribosyl cyclase activity were measured in cells maintained in growth-arrested conditions and exposed to vehicle or TNF-α (10-40 ng/ml). TNF-α-induced induction of CD38 expression was greater in ASMA than in ASM cells from nonasthmatic donors (ASMNA). In four of the six donors, basal and TNF-α-induced ERK and p38 MAPK activation were higher in ASMA than ASMNA cells. JNK MAPK activation was lower in ASMA than ASMNA cells. Nuclear NF-κB (p50 subunit) and phosphorylated c-Jun were comparable in cells from both groups, although nuclear c-Fos (part of the AP-1 complex) levels were lower in ASMA than ASMNA cells. NF-κB or AP-1 binding to their consensus sequences was comparable in ASMNA and ASMA cells, as are the decay kinetics of CD38 mRNA. The findings suggest that the differential induction of CD38 by TNF-α in ASMA cells is due to increased transcriptional regulation involving ERK and p38 MAPK activation and is independent of changes in NF-κB or AP-1 activation. The findings suggest a potential role for CD38 in the pathophysiology of asthma.
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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.