ArticleAmerican journal of physiology. Cell physiology2014
Activation of Notch signaling by short-term treatment with Jagged-1 enhances store-operated Ca(2+) entry in human pulmonary arterial smooth muscle cells.
Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 40 citations in OpenAlex.
- Notch1 regulates Orai1 and Orai3 expression in breast cancer cells.Scientific reports · 2025Article
- Piezo1 in heart failure: A new perspective from cytomechanical sensing to diverse cellular pathways.Molecular biology reports · 2025Review
- NOTCH3 and Pulmonary Arterial Hypertension.International journal of molecular sciences · 2024Review
- Synthetic Biology Meets CaCells · 2024Review
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- Jagged/Notch proteins promote endothelial-mesenchymal transition-mediated pulmonary arterial hypertension via upregulation of the expression of GATAs.Journal of cellular and molecular medicine · 2023Article
- Mechanosensitive channel Piezo1 is required for pulmonary artery smooth muscle cell proliferation.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Put in a "CaCells · 2022Review
- Endothelial upregulation of mechanosensitive channel Piezo1 in pulmonary hypertension.American journal of physiology. Cell physiology · 2021Article
- Neonatal Anesthesia by Ketamine in Neonatal Rats Inhibits the Proliferation and Differentiation of Hippocampal Neural Stem Cells and Decreases Neurocognitive Function in Adulthood via Inhibition of the Notch1 Signaling Pathway.Molecular neurobiology · 2021Article
- Halofuginone, a promising drug for treatment of pulmonary hypertension.British journal of pharmacology · 2021Article
- Pediatric Pulmonary Hypertension: Definitions, Mechanisms, Diagnosis, and Treatment.Comprehensive Physiology · 2021Article
- Astragaloside IV attenuates hypoxia‑induced pulmonary vascular remodeling via the Notch signaling pathway.Molecular medicine reports · 2021Article
- Notch enhances CaAmerican journal of physiology. Cell physiology · 2020Article
- Medicinal Plants and Phytochemicals for the Treatment of Pulmonary Hypertension.Frontiers in pharmacology · 2020Review
- Notch3 signalling and vascular remodelling in pulmonary arterial hypertension.Clinical science (London, England : 1979) · 2019Review
- Influence of the Assembly State on the Functionality of a Supramolecular Jagged1-Mimicking Peptide Additive.ACS omega · 2019Article
- Hypoxia selectively upregulates cation channels and increases cytosolic [CaAmerican journal of physiology. Cell physiology · 2018Article
- Induced pluripotent stem cell modelling of HLHS underlines the contribution of dysfunctional NOTCH signalling to impaired cardiogenesis.Human molecular genetics · 2017Article
- Selective regulation of Notch ligands during angiogenesis is mediated by vimentin.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Notch signaling plays a critical role in controlling proliferation and differentiation of pulmonary arterial smooth muscle cells (PASMC). Upregulated Notch ligands and Notch3 receptors in PASMC have been reported to promote the development of pulmonary vascular remodeling in patients with pulmonary arterial hypertension (PAH) and in animals with experimental pulmonary hypertension. Activation of Notch receptors by their ligands leads to the cleavage of the Notch intracellular domain (NICD) to the cytosol by γ-secretase; NICD then translocates into the nucleus to regulate gene transcription. In this study, we examined whether short-term activation of Notch functionally regulates store-operated Ca(2+) entry (SOCE) in human PASMC. Treatment of PASMC with the active fragment of human Jagged-1 protein (Jag-1) for 15-60 min significantly increased the amplitude of SOCE induced by passive deletion of Ca(2+) from the intracellular stores, the sarcoplasmic reticulum (SR). The Jag-1-induced enhancement of SOCE was time dependent: the amplitude was maximized at 30 min of treatment with Jag-1, which was closely correlated with the time course of Jag-1-mediated increase in NICD protein level. The scrambled peptide of Jag-1 active fragment had no effect on SOCE. Inhibition of γ-secretase by N-[N-(3,5-difluorophenacetyl-L-alanyl)]-S-phenylglycine t-butyl ester (DAPT) significantly attenuated the Jag-1-induced augmentation of SOCE. In addition to the short-term effect, prolonged treatment of PASMC with Jag-1 for 48 h also markedly enhanced the amplitude of SOCE. These data demonstrate that short-term activation of Notch signaling enhances SOCE in PASMC; the NICD-mediated functional interaction with store-operated Ca(2+) channels (SOC) may be involved in the Jag-1-mediated enhancement of SOCE in human PASMC.
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