ArticleAmerican journal of physiology. Cell physiology2016
Endothelial mitochondria regulate the intracellular Ca2+ response to fluid shear stress.
Article in American journal of physiology. Cell physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- A Color-Tuning Bioluminescent Sensor (AmyLuc) for Real-Time Monitoring of Intracellular pH Dynamics in Cancer Cells.Analytical chemistry · 2026Article
- Mitochondrial-Endothelial Crosstalk in Cardiometabolic Disease: Mechanisms and Translational Opportunities in the Multi-omics Era.Reviews in cardiovascular medicine · 2026Review
- Shear stress-induced CaBiological research · 2026Article
- A systematic investigation of endothelial cell behavior under hydrostatic pressure.Scientific reports · 2025Article
- Laminar Flow Alters EV Composition in HUVECs: A Study of Culture Medium Optimization and Molecular Profiling of Vesicle Cargo.Small methods · 2025Article
- The relationship of redox signaling with the risk for atherosclerosis.Frontiers in pharmacology · 2024Review
- Endothelial cells differentially sense laminar and disturbed flows by altering the lipid order of their plasma and mitochondrial membranes.American journal of physiology. Cell physiology · 2023Article
- Modulation of the mitochondrial CaPhysiological reports · 2023Article
- Mitochondrial ATP Production is Required for Endothelial Cell Control of Vascular Tone.Function (Oxford, England) · 2023Article
- The mitochondrial CaScientific reports · 2022Article
- Sex-Specific Differences in Endothelial Function Are Driven by Divergent Mitochondrial CaJournal of the American Heart Association · 2022Article
- A mitochondrial contribution to anti-inflammatory shear stress signaling in vascular endothelial cells.The Journal of cell biology · 2022Article
- Altered Mitochondrial Opa1-Related Fusion in Mouse Promotes Endothelial Cell Dysfunction and Atherosclerosis.Antioxidants (Basel, Switzerland) · 2022Article
- Early Inactivation of Membrane Estrogen Receptor Alpha (ERα) Recapitulates the Endothelial Dysfunction of Aged Mouse Resistance Arteries.International journal of molecular sciences · 2022Article
- Molecular nature and physiological role of the mitochondrial calcium uniporter channel.American journal of physiology. Cell physiology · 2021Review
- Mechanical forces and metabolic changes cooperate to drive cellular memory and endothelial phenotypes.Current topics in membranes · 2021Review
- Vessel-on-a-chip models for studying microvascular physiology, transport, and function in vitro.American journal of physiology. Cell physiology · 2021Review
- Shear stress activates mitochondrial oxidative phosphorylation by reducing plasma membrane cholesterol in vascular endothelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Modeling the role of endoplasmic reticulum-mitochondria microdomains in calcium dynamics.Scientific reports · 2019Article
- Restriction of mitochondrial calcium overload byBiology open · 2019Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Shear stress is known to stimulate an intracellular free calcium concentration ([Ca(2+)]i) response in vascular endothelial cells (ECs). [Ca(2+)]i is a key second messenger for signaling that leads to vasodilation and EC survival. Although it is accepted that the shear-induced [Ca(2+)]i response is, in part, due to Ca(2+) release from the endoplasmic reticulum (ER), the role of mitochondria (second largest Ca(2+) store) is unknown. We hypothesized that the mitochondria play a role in regulating [Ca(2+)]i in sheared ECs. Cultured ECs, loaded with a Ca(2+)-sensitive fluorophore, were exposed to physiological levels of shear stress. Shear stress elicited [Ca(2+)]i transients in a percentage of cells with a fraction of them displaying oscillations. Peak magnitudes, percentage of oscillating ECs, and oscillation frequencies depended on the shear level. [Ca(2+)]i transients/oscillations were present when experiments were conducted in Ca(2+)-free solution (plus lanthanum) but absent when ECs were treated with a phospholipase C inhibitor, suggesting that the ER inositol 1,4,5-trisphosphate receptor is responsible for the [Ca(2+)]i response. Either a mitochondrial uncoupler or an electron transport chain inhibitor, but not a mitochondrial ATP synthase inhibitor, prevented the occurrence of transients and especially inhibited the oscillations. Knockdown of the mitochondrial Ca(2+) uniporter also inhibited the shear-induced [Ca(2+)]i transients/oscillations compared with controls. Hence, EC mitochondria, through Ca(2+) uptake/release, regulate the temporal profile of shear-induced ER Ca(2+) release. [Ca(2+)]i oscillation frequencies detected were within the range for activation of mechanoresponsive kinases and transcription factors, suggesting that dysfunctional EC mitochondria may contribute to cardiovascular disease by deregulating the shear-induced [Ca(2+)]i response.
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Registered trials
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