ArticleBMC surgery2013
Ca²⁺-dependent nitric oxide release in the injured endothelium of excised rat aorta: a promising mechanism applying in vascular prosthetic devices in aging patients.
Article in BMC surgery, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
- Semiconducting Polymer Nanoparticles Enable Light-Controlled Bidirectional Modulation of Nitric Oxide in Endothelial Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Functional Coupling Between Voltage-Dependent Sodium Channels and Activation of the CaInternational journal of molecular sciences · 2026Article
- The Emerging Role of Endothelial Ion Channels in the Control of Human Microcirculation.International journal of molecular sciences · 2026Review
- Piezo1-related physiological and pathological processes in glioblastoma.Frontiers in cell and developmental biology · 2025Review
- The ion transport, GPCR, and RTK toolkit expression in the human cerebrovascular endothelial cell line, hCMEC/D3: an Omics perspective.Frontiers in physiology · 2025Article
- A new oxime synthesized fromRSC advances · 2024Article
- Opening of Cx43-formed hemichannels mediates the CaBiology direct · 2023Article
- An automated method to discover true events and classification of intracellular CaFrontiers in physiology · 2023Article
- Stable Gastric Pentadecapeptide BPC 157 and Wound Healing.Frontiers in pharmacology · 2021Review
- Group 1 metabotropic glutamate receptors trigger glutamate-induced intracellular CaCellular and molecular life sciences : CMLS · 2020Article
- Counteraction of perforated cecum lesions in rats: Effects of pentadecapeptide BPC 157, L-NAME and L-arginine.World journal of gastroenterology · 2018Article
- Bypassing major venous occlusion and duodenal lesions in rats, and therapy with the stable gastric pentadecapeptide BPC 157, L-NAME and L-arginine.World journal of gastroenterology · 2018Article
- Automated Intracellular Calcium Profiles Extraction from Endothelial Cells Using Digital Fluorescence Images.International journal of molecular sciences · 2018Article
- The Role of Endothelial CaInternational journal of molecular sciences · 2018Review
- Endothelial CaInternational journal of molecular sciences · 2018Review
- Stable gastric pentadecapeptide BPC 157 in the treatment of colitis and ischemia and reperfusion in rats: New insights.World journal of gastroenterology · 2017Article
- Celecoxib-induced gastrointestinal, liver and brain lesions in rats, counteraction by BPC 157 or L-arginine, aggravation by L-NAME.World journal of gastroenterology · 2017Article
- Follow-up of surgical and minimally invasive treatment of Achilles tendon pathology: a brief diagnostic imaging review.Musculoskeletal surgery · 2017Review
- Imaging of post-surgical treatment and of related complications in spinal trauma.Musculoskeletal surgery · 2017Review
- Cell Based Therapeutic Approach in Vascular Surgery: Application and Review.Open medicine (Warsaw, Poland) · 2017Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNitric oxide is key to endothelial regeneration, but it is still unknown whether endothelial cell (EC) loss results in an increase in NO levels at the wound edge. We have already shown that endothelial damage induces a long-lasting Ca²⁺ entry into surviving cells though connexin hemichannels (CxHcs) uncoupled from their counterparts on ruptured cells. The physiological outcome of injury-induced Ca²⁺ inflow is, however, unknown.
methodsIn this study, we sought to determine whether and how endothelial scraping induces NO production (NOP) in the endothelium of excised rat aorta by exploiting the NO-sensitive fluorochrome, DAF-FM diacetate and the Ca²⁺-sensitive fluorescent dye, Fura-2/AM.
resultsWe demonstrated that injury-induced NOP at the lesion site is prevented in presence of the endothelial NO synthase inhibitor, L-NAME, and in absence of extracellular Ca²⁺. Unlike ATP-dependent NO liberation, the NO response to injury is insensitive to BTP-2, which selectively blocks store-operated Ca²⁺ inflow. However, injury-induced NOP is significantly reduced by classic gap junction blockers, and by connexin mimetic peptides specifically targeting Cx37Hcs, Cx40HCs, and Cx43Hcs. Moreover, disruption of caveolar integrity prevents injury-elicited NO signaling, but not the accompanying Ca²⁺ response.
conclusionsThe data presented provide the first evidence that endothelial scraping stimulates NO synthesis at the wound edge, which might both exert an immediate anti-thrombotic and anti-inflammatory action and promote the subsequent re-endothelialization.
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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.