ArticleCellular and molecular bioengineering2014
Shear stress-induced NO production is dependent on ATP autocrine signaling and capacitative calcium entry.
Article in Cellular and molecular bioengineering, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
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- Membrane Cholesterol Interactions with Proteins in Hypercholesterolemia-Induced Endothelial Dysfunction.Current atherosclerosis reports · 2023Review
- Activating P2Y1 receptors improves function in arteries with repressed autophagy.Cardiovascular research · 2023Article
- TRPC channel-derived calcium fluxes differentially regulate ATP and flow-induced activation of eNOS.Nitric oxide : biology and chemistry · 2021Article
- Maternal Smoking Induced Cardiovascular Risks in Fetuses: How CanFrontiers in bioengineering and biotechnology · 2020Article
- Effect of spatial heterogeneity and colocalization of eNOS and capacitative calcium entry channels on shear stress-induced NO production by endothelial cells: A modeling approach.Cellular and molecular bioengineering · 2018Article
- Reduced membrane cholesterol after chronic hypoxia limits Orai1-mediated pulmonary endothelial CaAmerican journal of physiology. Heart and circulatory physiology · 2018Article
- Endothelial Cell Autophagy Maintains Shear Stress-Induced Nitric Oxide Generation via Glycolysis-Dependent Purinergic Signaling to Endothelial Nitric Oxide Synthase.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Reduced membrane cholesterol limits pulmonary endothelial CaAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Cholesterol Enrichment Impairs Capacitative Calcium Entry, eNOS Phosphorylation & Shear Stress-Induced NO Production.Cellular and molecular bioengineering · 2017Article
- Nitrite-Mediated Hypoxic Vasodilation Predicted from Mathematical Modeling and Quantified fromFrontiers in physiology · 2017Article
- The arterial microenvironment: the where and why of atherosclerosis.The Biochemical journal · 2016Review
- Endothelial mitochondria regulate the intracellular Ca2+ response to fluid shear stress.American journal of physiology. Cell physiology · 2016Article
- Mathematical model for shear stress dependent NO and adenine nucleotide production from endothelial cells.Nitric oxide : biology and chemistry · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Flow-induced production of nitric oxide (NO) by endothelial cells plays a fundamental role in vascular homeostasis. However, the mechanisms by which shear stress activates NO production remain unclear due in part to limitations in measuring NO, especially under flow conditions. Shear stress elicits the release of ATP, but the relative contribution of autocrine stimulation by ATP to flow-induced NO production has not been established. Furthermore, the importance of calcium in shear stress-induced NO production remains controversial, and in particular the role of capacitive calcium entry (CCE) has yet to be determined. We have utilized our unique NO measurement device to investigate the role of ATP autocrine signaling and CCE in shear stress-induced NO production. We found that endogenously released ATP and downstream activation of purinergic receptors and CCE plays a significant role in shear stress-induced NO production. ATP-induced eNOS phophorylation under static conditions is also dependent on CCE. Inhibition of protein kinase C significantly inhibited eNOS phosphorylation and the calcium response. To our knowledge, we are the first to report on the role of CCE in the mechanism of acute shear stress-induced NO response. In addition, our work highlights the importance of ATP autocrine signaling in shear stress-induced NO production.
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Registered trials
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