ArticleThe Journal of physiology2013
Role of microprojections in myoendothelial feedback--a theoretical study.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- The conducted vasomotor response and the principles of electrical communication in resistance arteries.Physiological reviews · 2024Review
- Notch Signaling in Vascular Endothelial and Mural Cell Communications.Cold Spring Harbor perspectives in medicine · 2022Article
- Functional Interaction among KInternational journal of molecular sciences · 2019Review
- Vasoconstrictor stimulus determines the functional contribution of myoendothelial feedback to mesenteric arterial tone.The Journal of physiology · 2018Article
- TRPV4 (Transient Receptor Potential Vanilloid 4) Channel-Dependent Negative Feedback Mechanism Regulates GArteriosclerosis, thrombosis, and vascular biology · 2018Article
- Notch Signaling in Endothelial Cells: Is It the Therapeutic Target for Vascular Neointimal Hyperplasia?International journal of molecular sciences · 2017Review
- Communication Is Key: Mechanisms of Intercellular Signaling in Vasodilation.Journal of cardiovascular pharmacology · 2017Review
- Can endothelial hemoglobin-α regulate nitric oxide vasodilatory signaling?American journal of physiology. Heart and circulatory physiology · 2017Article
- Calcium and electrical signaling in arterial endothelial tubes: New insights into cellular physiology and cardiovascular function.Microcirculation (New York, N.Y. : 1994) · 2017Review
- Stochastic model of endothelial TRPV4 calcium sparklets: effect of bursting and cooperativity on EDH.Biophysical journal · 2015Article
- Integration and Modulation of Intercellular Signaling Underlying Blood Flow Control.Journal of vascular research · 2015Article
- Notch signal integration in the vasculature during remodeling.Vascular pharmacology · 2014Review
- Less is more: minimal expression of myoendothelial gap junctions optimizes cell-cell communication in virtual arterioles.The Journal of physiology · 2014Article
- Agmatine induced NO dependent rat mesenteric artery relaxation and its impairment in salt-sensitive hypertension.Nitric oxide : biology and chemistry · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
We investigated the role of myoendothelial projections (MPs) in endothelial cell (EC) feedback response to smooth muscle cell (SMC) stimulation using mathematical modelling. A previously developed compartmental EC-SMC model is modified to include MPs as subcellular compartments in the EC. The model is further extended into a 2D continuum model using a finite element method (FEM) approach and electron microscopy images to account for MP geometry. The EC and SMC are coupled via non-selective myoendothelial gap junctions (MEGJs) which are located on MPs and allow exchange of Ca(2+), K(+), Na(+) and Cl(-) ions and inositol 1,4,5-triphosphate (IP3). Models take into consideration recent evidence for co-localization of intermediate-conductance calcium-activated potassium channels (IKCa) and IP3 receptors (IP3Rs) in the MPs. SMC stimulation causes an IP3-mediated Ca(2+) transient in the MPs with limited global spread in the bulk EC. A hyperpolarizing feedback generated by the localized IKCa channels is transmitted to the SMC via MEGJs. MEGJ resistance (Rgj) and the density of IKCa and IP3R in the projection influence the extent of EC response to SMC stimulation. The predicted Ca(2+) transients depend also on the volume and geometry of the MP. We conclude that in the myoendothelial feedback response to SMC stimulation, MPs are required to amplify the SMC initiated signal. Simulations suggest that the signal is mediated by IP3 rather than Ca(2+) diffusion and that a localized rather than a global EC Ca(2+) mobilization is more likely following SMC stimulation.
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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.