ArticleScientific reports2016
Mechanical perturbations trigger endothelial nitric oxide synthase activity in human red blood cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- Effect of Remote Ischemic Conditioning and Red Blood Cells Biomarkers on Outcomes in Patients With Acute Stroke.Journal of the American Heart Association · 2025Trial
- Trial
- Elemental analysis in menstrual effluent of women with PCOS: association with oxidative stress mechanisms: a case-control study.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
- SIRPα extracellular domain shed from neutrophils by ADAM10 aggravates sepsis via initiating nitric oxide release from erythrocyte.Journal of advanced research · 2026Article
- Article
- Emerging concepts in the molecular cell biology and functions of mammalian erythrocytes.The Journal of biological chemistry · 2025Review
- Erythrocytes enhance oxygen-carrying capacity through self-regulation.Frontiers in physiology · 2025Review
- Photobiomodulation and nitric oxide signaling.Nitric oxide : biology and chemistry · 2023Review
- Cellular microdomains for nitric oxide signaling in endothelium and red blood cells.Nitric oxide : biology and chemistry · 2020Review
- Nuclear factor-kB and nitric oxide synthases in red blood cells: good or bad in obesity? A preliminary study.European journal of histochemistry : EJH · 2020Article
- Hydrodynamic shear stress promotes epithelial-mesenchymal transition by downregulating ERK and GSK3β activities.Breast cancer research : BCR · 2019Article
- The ATP-binding cassette transporter A1 regulates phosphoantigen release and Vγ9Vδ2 T cell activation by dendritic cells.Nature communications · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO), a vascular signaling molecule, is primarily produced by endothelial NO synthase. Recently, a functional endothelial NO synthase (eNOS) was described in red blood cells (RBC). The RBC-eNOS contributes to the intravascular NO pool and regulates physiological functions. However the regulatory mechanisms and clinical implications of RBC-eNOS are unknown. The present study investigated regulation and functions of RBC-eNOS under mechanical stimulation. This study shows that mechanical stimuli perturb RBC membrane, which triggers a signaling cascade to activate the eNOS. Extracellular NO level, estimated by the 4-Amino-5-Methylamino-2', 7'-Difluorofluorescein Diacetate probe, was significantly increased under mechanical stimuli. Immunostaining and western blot studies confirmed that the mechanical stimuli phosphorylate the serine 1177 moiety of RBC-eNOS, and activates the enzyme. The NO produced by activation of RBC-eNOS in vortexed RBCs promoted important endothelial functions such as migration and vascular sprouting. We also show that mechanical perturbation facilitates nitrosylation of RBC proteins via eNOS activation. The results of the study confirm that mechanical perturbations sensitize RBC-eNOS to produce NO, which ultimately defines physiological boundaries of RBC structure and functions. Therefore, we propose that mild physical perturbations before, after, or during storage can improve viability of RBCs in blood banks.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.