ArticleBiochimica et biophysica acta2016
Two functionally distinct pools of eNOS in endothelium are facilitated by myoendothelial junction lipid composition.
Article in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Arterial iron regulates vasodilation during anemia via endothelial holo-alpha globin.bioRxiv : the preprint server for biology · 2025Article
- Elastin Regulation of Vasoreactivity in Resistance Arteries.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Impact of Endothelial Diversity and Dysfunction on Cardiovascular Disease.Comprehensive Physiology · 2025Review
- Sickle Trait and Alpha Thalassemia Increase NOS-Dependent Vasodilation of Human Arteries Through Disruption of Endothelial Hemoglobin-eNOS Interactions.Circulation · 2025Article
- Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024Review
- Myoendothelial feedback in mouse mesenteric resistance arteries is similar between the sexes, dependent on nitric oxide synthase, and independent of TPRV4.American journal of physiology. Heart and circulatory physiology · 2024Article
- The conducted vasomotor response and the principles of electrical communication in resistance arteries.Physiological reviews · 2024Review
- Article
- Redox-Regulation of α-Globin in Vascular Physiology.Antioxidants (Basel, Switzerland) · 2022Article
- Red Blood Cell and Endothelial eNOS Independently Regulate Circulating Nitric Oxide Metabolites and Blood Pressure.Circulation · 2021Article
- Redox Switches Controlling Nitric Oxide Signaling in the Resistance Vasculature and Implications for Blood Pressure Regulation: Mid-Career Award for Research Excellence 2020.Hypertension (Dallas, Tex. : 1979) · 2021Review
- Polarized Proteins in Endothelium and Their Contribution to Function.Journal of vascular research · 2021Review
- Group 1 metabotropic glutamate receptors trigger glutamate-induced intracellular CaCellular and molecular life sciences : CMLS · 2020Article
- Cellular microdomains for nitric oxide signaling in endothelium and red blood cells.Nitric oxide : biology and chemistry · 2020Review
- Myoendothelial Junctions of Mature Coronary Vessels Express Notch Signaling Proteins.Frontiers in physiology · 2020Article
- S-nitrosoglutathione inhibits cerebrovascular angiotensin II-dependent and -independent ATBritish journal of pharmacology · 2019Article
- Escorting α-globin to eNOS: α-globin-stabilizing protein paves the way.The Journal of clinical investigation · 2018Article
- Non-Endoplasmic Reticulum-Based Calr (Calreticulin) Can Coordinate Heterocellular Calcium Signaling and Vascular Function.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Nonylphenol and Octylphenol Differently Affect Cell Redox Balance by Modulating the Nitric Oxide Signaling.Oxidative medicine and cellular longevity · 2018Article
- Redox Control of Vascular Function.Arteriosclerosis, thrombosis, and vascular biology · 2017Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
In resistance arteries, endothelial cells (EC) make contact with smooth muscle cells (SMC), forming myoendothelial junctions (MEJ). Endothelial nitric oxide synthase (eNOS) is present in the luminal side of the EC (apical EC) and the basal side of the EC (MEJ). To test if these eNOS pools acted in sync or separately, we co-cultured ECs and SMCs, then stimulated SMCs with phenylephrine (PE). Adrenergic activation causes inositol [1,4,5] triphosphate (IP3) to move from SMC to EC through gap junctions at the MEJ. PE increases MEJ eNOS phosphorylation (eNOS-P) at S1177, but not in EC. Conversely, we used bradykinin (BK) to increase EC calcium; this increased EC eNOS-P but did not affect MEJ eNOS-P. Inhibiting gap junctions abrogated the MEJ eNOS-P after PE, but had no effect on BK eNOS-P. Differential lipid composition between apical EC and MEJ may account for the compartmentalized eNOS-P response. Indeed, DAG and phosphatidylserine are both enriched in MEJ. These lipids are cofactors for PKC activity, which was significantly increased at the MEJ after PE. Because PKC activity also relies on endoplasmic reticulum (ER) calcium release, we used thapsigargin and xestospongin C, BAPTA, and PKC inhibitors, which caused significant decreases in MEJ eNOS-P after PE. Functionally, BK inhibited leukocyte adhesion and PE caused an increase in SMC cGMP. We hypothesize that local lipid composition of the MEJ primes PKC and eNOS-P for stimulation by PE, allowing for compartmentalized function of eNOS in the blood vessel wall.
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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.