ArticleHypertension (Dallas, Tex. : 1979)2011
Activation of NADPH oxidase 1 increases intracellular calcium and migration of smooth muscle cells.
Article in Hypertension (Dallas, Tex. : 1979), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 54 citations in OpenAlex.
- Novel Drug-Testing Platform for Vascular Injury-induced Intimal Hyperplasia Using a Microphysiological System.Advanced healthcare materials · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Nox1/PAK1 is required for angiotensin II-induced vascular inflammation and abdominal aortic aneurysm formation.Redox biology · 2025Article
- A Novel PPARγ Modulator Falcarindiol Mediates ER Stress-Mediated Apoptosis by Regulating NOX4 and Overcomes Radioresistance in Breast Cancer.Antioxidants (Basel, Switzerland) · 2024Article
- Oxidative Stress in Kidney Injury and Hypertension.Antioxidants (Basel, Switzerland) · 2024Review
- Nodakenin Induces ROS-Dependent Apoptotic Cell Death and ER Stress in Radioresistant Breast Cancer.Antioxidants (Basel, Switzerland) · 2023Article
- Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022Review
- Navigating Calcium and Reactive Oxygen Species by Natural Flavones for the Treatment of Heart Failure.Frontiers in pharmacology · 2021Review
- Cellular and Molecular Processes in Pulmonary Hypertension.Advances in experimental medicine and biology · 2021Article
- Quiescin/sulfhydryl oxidase 1b (QSOX1b) induces migration and proliferation of vascular smooth muscle cells by distinct redox pathways.Archives of biochemistry and biophysics · 2020Article
- Neutrophil Extracellular Traps Tied to Rheumatoid Arthritis: Points to Ponder.Frontiers in immunology · 2020Review
- Apoptosis signal-regulating kinase 1 activation by Nox1-derived oxidants is required for TNFα receptor endocytosis.American journal of physiology. Heart and circulatory physiology · 2019Article
- Redox Activation of Nox1 (NADPH Oxidase 1) Involves an Intermolecular Disulfide Bond Between Protein Disulfide Isomerase and p47Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Drebrin regulates angiotensin II-induced aortic remodelling.Cardiovascular research · 2018Article
- Matrix vesicles induce calcification of recipient vascular smooth muscle cells through multiple signaling pathways.Kidney international · 2018Article
- Intracellular calcium increases in vascular smooth muscle cells with progression of chronic kidney disease in a rat model.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017Article
- Reactive Oxygen Species Link Gonadotropin-Releasing Hormone Receptor Signaling Cascades in the Gonadotrope.Frontiers in endocrinology · 2017Article
- Calcium and ROS: A mutual interplay.Redox biology · 2015Review
- Phosphorylation of Nox1 regulates association with NoxA1 activation domain.Circulation research · 2014Article
- Nox NADPH oxidases and the endoplasmic reticulum.Antioxidants & redox signaling · 2014Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Redox-dependent migration and proliferation of vascular smooth muscle cells (SMCs) are central events in the development of vascular proliferative diseases; however, the underlying intracellular signaling mechanisms are not fully understood. We tested the hypothesis that activation of Nox1 NADPH oxidase modulates intracellular calcium ([Ca(2+)](i)) levels. Using cultured SMCs from wild-type and Nox1 null mice, we confirmed that thrombin-dependent generation of reactive oxygen species requires Nox1. Thrombin rapidly increased [Ca(2+)](i), as measured by fura-2 fluorescence ratio imaging, in wild-type but not Nox1 null SMCs. The increase in [Ca(2+)](i) in wild-type SMCs was inhibited by antisense to Nox1 and restored by expression of Nox1 in Nox1 null SMCs. Investigation into potential mechanisms by which Nox1 modulates [Ca(2+)](i) showed that thrombin-induced inositol triphosphate generation and thapsigargin-induced intracellular calcium mobilization were similar in wild-type and Nox1 null SMCs. To examine the effects of Nox1 on Ca(2+) entry, cells were either bathed in Ca(2+)-free medium or exposed to dihydropyridines to block L-type Ca(2+) channel activity. Treatment with nifedipine or removal of extracellular Ca(2+) reduced the thrombin-mediated increase of [Ca(2+)](i) in wild-type SMCs, whereas the response in Nox1 null SMCs was unchanged. Sodium vanadate, an inhibitor of protein tyrosine phosphatases, restored the thrombin-induced increase of [Ca(2+)](i) in Nox1 null SMCs. Migration of SMCs was impaired with deficiency of Nox1 and restored with expression of Nox1 or the addition of sodium vanadate. In summary, we conclude that Nox1 NADPH oxidase modulates Ca(2+) mobilization in SMCs, in part through regulation of Ca(2+) influx, to thereby promote cell migration.
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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.