ArticleAntioxidants & redox signaling2012
Redox regulation of SERCA2 is required for vascular endothelial growth factor-induced signaling and endothelial cell migration.
Article in Antioxidants & redox signaling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
- Effects of low-dose lithium supplementation on thermal inactivation of SERCA in cardiac muscle of male mice.Bioscience reports · 2026Article
- The potential impact of exosomal miR-484 on post-myocardial infarction angiogenesis using bioinformatics and experimental verification.BMC cardiovascular disorders · 2026Article
- Allosteric Modulation of SERCA Pumps in Health and Disease: Structural Dynamics, Posttranslational Modifications, and Therapeutic Potential.Journal of molecular biology · 2025Review
- Review
- ABCB5Stem cell research & therapy · 2023Article
- The Molecular Heterogeneity of Store-Operated CaInternational journal of molecular sciences · 2023Review
- GABACells · 2022Article
- Reactive Oxygen Species and Endothelial CaInternational journal of molecular sciences · 2021Review
- Expression of TSP50, SERCA2 and IL-8 in Colorectal Adenoma and Carcinoma: Correlation to Clinicopathological Factors.Pathology oncology research : POR · 2021Article
- Review
- S-glutathionylation, friend or foe in cardiovascular health and disease.Redox biology · 2020Review
- Role of Glutaredoxin-1 and Glutathionylation in Cardiovascular Diseases.International journal of molecular sciences · 2020Review
- Redox RegulationAntioxidants & redox signaling · 2020Review
- Endothelial cell-specific redox gene modulation inhibits angiogenesis but promotes B16F0 tumor growth in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Cysteine Glutathionylation Acts as a Redox Switch in Endothelial Cells.Antioxidants (Basel, Switzerland) · 2019Review
- Endothelial CaInternational journal of molecular sciences · 2019Review
- Endothelial Transient Receptor Potential Channels and Vascular Remodeling: Extracellular CaFrontiers in physiology · 2019Review
- HAX-1 regulates SERCA2a oxidation and degradation.Journal of molecular and cellular cardiology · 2018Article
- SERCA directs cell migration and branching across species and germ layers.Biology open · 2017Article
- European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS).Redox biology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
aimsVascular endothelial growth factor (VEGF) increases angiogenesis by stimulating endothelial cell (EC) migration. VEGF-induced nitric oxide ((•)NO) release from (•)NO synthase plays a critical role, but the proteins and signaling pathways that may be redox-regulated are poorly understood. The aim of this work was to define the role of (•)NO-mediated redox regulation of the sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA) in VEGF-induced signaling and EC migration.
resultsVEGF-induced EC migration was prevented by the (•)NO synthase inhibitor, N (G)-nitro-L-arginine methyl ester (LNAME). Either VEGF or (•)NO stimulated endoplasmic reticulum (ER) (45)Ca(2+) uptake, a measure of SERCA activity, and knockdown of SERCA2 prevented VEGF-induced EC migration and (45)Ca(2+) uptake. S-glutathione adducts on SERCA2b, identified immunochemically, were increased by VEGF, and were prevented by LNAME or overexpression of glutaredoxin-1 (Glrx-1). Furthermore, VEGF failed to stimulate migration of ECs overexpressing Glrx-1. VEGF or (•)NO increased SERCA S-glutathiolation and stimulated migration of ECs in which wild-type (WT) SERCA2b was overexpressed with an adenovirus, but did neither in those overexpressing a C674S SERCA2b mutant, in which the reactive cysteine-674 was mutated to a serine. Increased EC Ca(2+) influx caused by VEGF or (•)NO was abrogated by overexpression of Glrx-1 or the C674S SERCA2b mutant. ER store-emptying through the ryanodine receptor (RyR) and Ca(2+) entry through Orai1 were also required for VEGF- and (•)NO-induced EC Ca(2+) influx. INNOVATION AND
conclusionsThese results demonstrate that (•)NO-mediated activation of SERCA2b via S-glutathiolation of cysteine-674 is required for VEGF-induced EC Ca(2+) influx and migration, and establish redox regulation of SERCA2b as a key component in angiogenic signaling.
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Registered trials
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