ArticlePflugers Archiv : European journal of physiology2012
Airway smooth muscle STIM1 and Orai1 are upregulated in asthmatic mice and mediate PDGF-activated SOCE, CRAC currents, proliferation, and migration.
Article in Pflugers Archiv : European journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 86 citations in OpenAlex.
- lncRNA HOTAIR promotes airway remodeling by regulating metabolic reprogramming through the FUS/HK2 axis in airway smooth muscle cells.Molecular biology reports · 2026Article
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Orai storeoperated CaChannels (Austin, Tex.) · 2025Review
- Is the SPLUNC1-Orai1 axis a critical determinant of lung health?Biochemical Society transactions · 2025Review
- Ion Channels in the Immune Response of Asthma.Journal of respiratory biology and translational medicine · 2024Article
- Circular RNAs in human diseases.MedComm · 2024Review
- Role of STIM1 in stretch-induced signaling in human airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Characterization of PDGF-Induced Subcellular Calcium Regulation through Calcium Channels in Airway Smooth Muscle Cells by FRET Biosensors.Biosensors · 2024Article
- Calcium Signaling in Airway Epithelial Cells: Current Understanding and Implications for Inflammatory Airway Disease.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Too much of a good thing: The case of SOCE in cellular apoptosis.Cell calcium · 2023Review
- Airway Smooth Muscle Regulated by Oxidative Stress in COPD.Antioxidants (Basel, Switzerland) · 2023Review
- A review of the pathophysiology and the role of ion channels on bronchial asthma.Frontiers in pharmacology · 2023Review
- Circular RNAs: emerging players in asthma and COPD.Frontiers in cell and developmental biology · 2023Review
- Super resolution microscopy analysis reveals increased Orai1 activity in asthma and cystic fibrosis lungs.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2023Article
- Airway smooth muscle in contractility and remodeling of asthma: potential drug target mechanisms.Expert opinion on therapeutic targets · 2023Article
- The Regulatory Role of miR-107-Cdk6-Rb Pathway in Airway Smooth Muscle Cells in Asthma.Journal of asthma and allergy · 2023Article
- Inherent differences of small airway contraction and CaFrontiers in cell and developmental biology · 2023Article
- STIM1 is the key that unlocks airway smooth muscle remodeling and hyperresponsiveness during asthma.Cell calcium · 2022Article
- STIM1 is a core trigger of airway smooth muscle remodeling and hyperresponsiveness in asthma.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- IL-13 Regulates Orai1 Expression in Human Bronchial Smooth Muscle Cells and Airway Remodeling in Asthma Mice Model via LncRNA H19.Journal of asthma and allergy · 2022Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Airway smooth muscle cell (ASMC) remodeling contributes to the structural changes in the airways that are central to the clinical manifestations of asthma. Ca(2+) signals play an important role in ASMC remodeling through control of ASMC migration and hypertrophy/proliferation. Upregulation of STIM1 and Orai1 proteins, the molecular components of the store-operated Ca(2+) entry (SOCE) pathway, has recently emerged as an important mediator of vascular remodeling. However, the potential upregulation of STIM1 and Orai1 in asthmatic airways remains unknown. An important smooth muscle migratory agonist with major contributions to ASMC remodeling is the platelet-derived growth factor (PDGF). Nevertheless, the Ca(2+) entry route activated by PDGF in ASMC remains elusive. Here, we show that STIM1 and Orai1 protein levels are greatly upregulated in ASMC isolated from ovalbumin-challenged asthmatic mice, compared to control mice. Furthermore, we show that PDGF activates a Ca(2+) entry pathway in rat primary ASMC that is pharmacologically reminiscent of SOCE. Molecular knockdown of STIM1 and Orai1 proteins inhibited PDGF-activated Ca(2+) entry in these cells. Whole-cell patch clamp recordings revealed the activation of Ca(2+) release-activated Ca(2+) (CRAC) current by PDGF in ASMC. These CRAC currents were abrogated upon either STIM1 or Orai1 knockdown. We show that either STIM1 or Orai1 knockdown significantly inhibited ASMC proliferation and chemotactic migration in response to PDGF. These results implicate STIM1 and Orai1 in PDGF-induced ASMC proliferation and migration and suggest the potential use of STIM1 and Orai1 as targets for ASMC remodeling during 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.