ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Knockdown of stromal interaction molecule 1 attenuates store-operated Ca2+ entry and Ca2+ responses to acute hypoxia in pulmonary arterial smooth muscle.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 80 citations in OpenAlex.
- Crosstalk between calcium and reactive oxygen species signaling in cancer revisited.Cell calcium · 2025Review
- SARS-CoV-2 spike protein receptor-binding domain perturbates intracellular calcium homeostasis and impairs pulmonary vascular endothelial cells.Signal transduction and targeted therapy · 2023Article
- Acute oxygen sensing by vascular smooth muscle cells.Frontiers in physiology · 2023Review
- The STIM1/2-Regulated Calcium Homeostasis Is Impaired in Hippocampal Neurons of the 5xFAD Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2022Article
- Crucial Role of Stromal Interaction Molecule-Activated TRPC-ORAI Channels in Vascular Remodeling and Pulmonary Hypertension Induced by Intermittent Hypoxia.Frontiers in physiology · 2022Article
- Interrelation between ROS and CaRedox biology · 2020Review
- Tetramethylpyrazine: A promising drug for the treatment of pulmonary hypertension.British journal of pharmacology · 2020Article
- Cytochrome P450 Epoxygenase-Dependent Activation of TRPV4 Channel Participates in Enhanced Serotonin-Induced Pulmonary Vasoconstriction in Chronic Hypoxic Pulmonary Hypertension.Analytical cellular pathology (Amsterdam) · 2020Article
- Interplay between ER CaInternational journal of molecular sciences · 2018Article
- Molecular physiology and pathophysiology of stromal interaction molecules.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- Revisiting the Role of TRP, Orai, and ASIC Channels in the Pulmonary Arterial Response to Hypoxia.Frontiers in physiology · 2018Review
- STIM2 regulates both intracellular CaScientific reports · 2017Article
- Isolation, culture and identification of pulmonary arterial smooth muscle cells from rat distal pulmonary arteries.Cytotechnology · 2017Article
- BTP2, a Store-Operated Calcium Channel Inhibitor, Attenuates Lung Ischemia-Reperfusion Injury in Rats.Inflammation · 2017Article
- Role of STIM2 in cell function and physiopathology.The Journal of physiology · 2017Review
- Crosstalk between calcium and reactive oxygen species signaling in cancer.Cell calcium · 2017Review
- Notch activation of CaHypertension research : official journal of the Japanese Society of Hypertension · 2017Article
- Orai1, 2, 3 and STIM1 promote store-operated calcium entry in pulmonary arterial smooth muscle cells.Cell death discovery · 2017Article
- STIM1, a direct target of microRNA-185, promotes tumor metastasis and is associated with poor prognosis in colorectal cancer.Oncogene · 2015Article
- Notch Activation of Ca(2+) Signaling in the Development of Hypoxic Pulmonary Vasoconstriction and Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2015Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Stromal interaction molecule 1 (STIM1) is a recently discovered membrane-spanning protein thought to sense lumenal Ca(2+) in sarco(endo)plasmic reticulum (SR/ER) and transduce activation of Ca(2+)-permeable store-operated channels (SOC) in plasmalemma in response to SR/ER Ca(2+) depletion. To evaluate the role of STIM1 and a closely related protein, STIM2, in Ca(2+) signaling of rat distal pulmonary arterial smooth muscle cells (PASMC) during hypoxia, we used fluorescent microscopy and the Ca(2+)-sensitive dye, fura 2, to measure basal intracellular Ca(2+) concentration ([Ca(2+)](i)), store-operated Ca(2+) entry (SOCE), and increases in [Ca(2+)](i) caused by acute hypoxia (4% O(2)) or depolarization (60 mmol/l KCl) in cells treated with small interfering RNA targeted to STIM1 (siSTIM1) or STIM2 (siSTIM2). As determined by real-time quantitative PCR analysis (qPCR), STIM1 mRNA was 200-fold more abundant than STIM2 in untreated control PASMC. siSTIM1 and siSTIM2 caused specific and significant knockdown of both mRNA measured by qPCR and protein measured by Western blotting. siSTIM1 markedly inhibited SOCE and abolished the sustained [Ca(2+)](i) response to hypoxia but did not alter the initial transient [Ca(2+)](i) response to hypoxia, the [Ca(2+)](i) response to depolarization, or basal [Ca(2+)](i). The only effect of siSTIM2 was a smaller inhibition of SOCE. We conclude that STIM1 was quantitatively more important than STIM2 in activation of SOC in rat distal PASMC and that the increase in [Ca(2+)](i) induced by acute hypoxia in these cells required SR Ca(2+) release and STIM1-dependent activation of SOC.
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