ArticleJournal of cellular physiology2015
S-nitrosylation of Cofilin-1 Serves as a Novel Pathway for VEGF-Stimulated Endothelial Cell Migration.
Article in Journal of cellular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Integrating machine learning and multi-omics analysis to reveal nucleotide metabolism-related immune genes and their functional validation in ischemic stroke.Frontiers in immunology · 2025Article
- Microglial activation induces nitric oxide signalling and alters protein S-nitrosylation patterns in extracellular vesicles.Journal of extracellular vesicles · 2024Article
- Effects of vitamin D signaling in cardiovascular disease: centrality of macrophage polarization.Frontiers in cardiovascular medicine · 2024Article
- Mapping Pregnancy-dependent Sulfhydrome Unfolds Diverse Functions of Protein Sulfhydration in Human Uterine Artery.Endocrinology · 2023Article
- The Role of Nrf2 in Relieving Cerebral Ischemia-Reperfusion Injury.Current neuropharmacology · 2023Review
- Intracellular Protein S-Nitrosylation-A Cells Response to Extracellular S100B and RAGE Receptor.Biomolecules · 2022Article
- Thiol Modifications in the Extracellular Space-Key Proteins in Inflammation and Viral Infection.Frontiers in immunology · 2022Review
- Nitric Oxide and Electrophilic Cyclopentenone Prostaglandins in Redox signaling, Regulation of Cytoskeleton Dynamics and Intercellular Communication.Frontiers in cell and developmental biology · 2021Review
- Estrogen Receptors and Estrogen-Induced Uterine Vasodilation in Pregnancy.International journal of molecular sciences · 2020Review
- Article
- Analysis of mesenchymal stem cell proteomesTheranostics · 2020Article
- Role of Cofilin in Alzheimer's Disease.Frontiers in cell and developmental biology · 2020Review
- Evidence against Stable Protein S-Nitrosylation as a Widespread Mechanism of Post-translational Regulation.Molecular cell · 2018Article
- VEGF Triggers the Activation of Cofilin and the Arp2/3 Complex within the Growth Cone.International journal of molecular sciences · 2018Article
- A Salutary Role of Reactive Oxygen Species in Intercellular Tunnel-Mediated Communication.Frontiers in cell and developmental biology · 2018Review
- Degradation of cofilin is regulated by Cbl, AIP4 and Syk resulting in increased migration of LMP2A positive nasopharyngeal carcinoma cells.Scientific reports · 2017Article
- Redox regulation of the actin cytoskeleton and its role in the vascular system.Free radical biology & medicine · 2017Review
- Cofilin-1 and Other ADF/Cofilin Superfamily Members in Human Malignant Cells.International journal of molecular sciences · 2016Review
- Quantitative Proteomics Analysis of VEGF-Responsive Endothelial Protein S-Nitrosylation Using Stable Isotope Labeling by Amino Acids in Cell Culture (SILAC) and LC-MS/MS.Biology of reproduction · 2016Article
- Nitric Oxide Modulates Postnatal Bone Marrow-Derived Mesenchymal Stem Cell Migration.Frontiers in cell and developmental biology · 2016Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Nitric oxide (NO) derived from endothelial NO synthase (eNOS) mediates vascular endothelial growth factor (VEGF)-stimulated endothelial cytoskeleton remodeling and migration; however, the underlying mechanisms are elusive. Covalent adduction of a NO moiety (NO(•)) to cysteines called S-nitrosylation (SNO) is a key NO signaling pathway. The small actin-binding protein cofilin-1 (CFL1) is essential for actin cytoskeleton remodeling. We investigated whether S-nitrosylation regulates CFL1 function and endothelial cytoskeleton remodeling and migration upon VEGF stimulation. VEGF rapidly stimulated S-nitrosylation of CFL1, which was blocked by NO Synthase inhibition and eNOS knockdown by specific eNOS-siRNA. Cys80 and Cys139 were identified as the major SNO-sites in CFL1 by LC-MS/MS. The actin severing activity of recombinant SNO-mimetic CFL1 (C80/139A DMA-CFL1), but not SNO-deficient CFL1 (C80/139S DMS-CFL1), was significantly greater than that of wild-type CFL1 (wt-CFL1). When wt-CFL1 and its mutants were overexpressed in endothelial cells, basal actin bound wt-CFL1 was undetectable but significantly increased by VEGF; basal actin bound DMA-CFL1 was readily high and basal actin bound DMS-CFL1 was detectable but low, and both were unresponsive to VEGF. Treatment with VEGF significantly increased filamentous (F-) actin and filopodium formation and cell migration in endothelial cells. Overexpression of wt-CFL1 inhibited VEGF-induced F-actin formation. Overexpression of DMA but not DMS CFL1 decreased basal but not VEGF-stimulated F-actin formation. Overexpression of DMA but not DMS CFL1 suppressed VEGF-stimulated filopodium formation and migration in endothelial cells. Thus, S-nitrosylation of CFL1 provides a novel signaling pathway post-NO biosynthesis via eNOS-derived NO for endothelial cytoskeleton remodeling and migration upon VEGF stimulation.
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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.