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6 results on '"Alevriadou, A"'

1. The mitochondrial Ca2+ uniporter channel synergizes with fluid shear stress to induce mitochondrial Ca2+ oscillations

Author

Akshar Patel, Matthew Simkulet, Soumya Maity, Manigandan Venkatesan, Anastasios Matzavinos, Muniswamy Madesh, and B. Rita Alevriadou

Subjects
Medicine, Science
Abstract

Abstract The mitochondrial calcium (Ca2+) uniporter (MCU) channel is responsible for mitochondrial Ca2+ influx. Its expression was found to be upregulated in endothelial cells (ECs) under cardiovascular disease conditions. Since the role of MCU in regulating cytosolic Ca2+ homeostasis in ECs exposed to shear stress (SS) is unknown, we studied mitochondrial Ca2+ dynamics (that is known to decode cytosolic Ca2+ signaling) in sheared ECs. To understand cause-and-effect, we ectopically expressed MCU in ECs. A higher percentage of MCU-transduced ECs exhibited mitochondrial Ca2+ transients/oscillations, and at higher frequency, under SS compared to sheared control ECs. Transients/oscillations correlated with mitochondrial reactive oxygen species (mROS) flashes and mitochondrial membrane potential (ΔΨm) flickers, and depended on activation of the mechanosensitive Piezo1 channel and the endothelial nitric oxide synthase (eNOS). A positive feedback loop composed of mitochondrial Ca2+ uptake/mROS flashes/ΔΨm flickers and endoplasmic reticulum Ca2+ release, in association with Piezo1 and eNOS, provided insights into the mechanism by which SS, under conditions of high MCU activity, may shape vascular EC energetics and function.

Published
2022
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4. The mitochondrial Ca

Author

Akshar, Patel, Matthew, Simkulet, Soumya, Maity, Manigandan, Venkatesan, Anastasios, Matzavinos, Muniswamy, Madesh, and B Rita, Alevriadou

Subjects
Endothelial Cells
Abstract

The mitochondrial calcium (Ca

Published
2022

5. The mitochondrial Ca2+ uniporter channel synergizes with fluid shear stress to induce mitochondrial Ca2+ oscillations.

Author

Patel, Akshar, Simkulet, Matthew, Maity, Soumya, Venkatesan, Manigandan, Matzavinos, Anastasios, Madesh, Muniswamy, and Alevriadou, B. Rita

Subjects
SHEARING force, MITOCHONDRIA, NITRIC-oxide synthases, OSCILLATIONS, REACTIVE oxygen species
Abstract

The mitochondrial calcium (Ca2+) uniporter (MCU) channel is responsible for mitochondrial Ca2+ influx. Its expression was found to be upregulated in endothelial cells (ECs) under cardiovascular disease conditions. Since the role of MCU in regulating cytosolic Ca2+ homeostasis in ECs exposed to shear stress (SS) is unknown, we studied mitochondrial Ca2+ dynamics (that is known to decode cytosolic Ca2+ signaling) in sheared ECs. To understand cause-and-effect, we ectopically expressed MCU in ECs. A higher percentage of MCU-transduced ECs exhibited mitochondrial Ca2+ transients/oscillations, and at higher frequency, under SS compared to sheared control ECs. Transients/oscillations correlated with mitochondrial reactive oxygen species (mROS) flashes and mitochondrial membrane potential (ΔΨm) flickers, and depended on activation of the mechanosensitive Piezo1 channel and the endothelial nitric oxide synthase (eNOS). A positive feedback loop composed of mitochondrial Ca2+ uptake/mROS flashes/ΔΨm flickers and endoplasmic reticulum Ca2+ release, in association with Piezo1 and eNOS, provided insights into the mechanism by which SS, under conditions of high MCU activity, may shape vascular EC energetics and function. [ABSTRACT FROM AUTHOR]

Published
2022
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6. Modeling the role of endoplasmic reticulum-mitochondria microdomains in calcium dynamics

Author

Nikolaos M. Tsoukias, Baarbod Ashenagar, B. Rita Alevriadou, and Arash Moshkforoush

Subjects
0301 basic medicine, chemistry.chemical_element, lcsh:Medicine, Calcium, Mitochondrion, Endoplasmic Reticulum, Models, Biological, Article, 03 medical and health sciences, chemistry.chemical_compound, Computational biophysics, 0302 clinical medicine, Cytosol, Animals, Humans, Inositol 1,4,5-Trisphosphate Receptors, Computational models, Calcium Signaling, Uniporter, lcsh:Science, Calcium signaling, Multidisciplinary, Endoplasmic reticulum, lcsh:R, Inositol trisphosphate, Compartment (chemistry), Models, Theoretical, Mitochondria, Calcium channels, 030104 developmental biology, chemistry, Biophysics, lcsh:Q, Biomedical engineering, 030217 neurology & neurosurgery
Abstract

Upon inositol trisphosphate (IP3) stimulation of non-excitable cells, including vascular endothelial cells, calcium (Ca2+) shuttling between the endoplasmic reticulum (ER) and mitochondria, facilitated by complexes called Mitochondria-Associated ER Membranes (MAMs), is known to play an important role in the occurrence of cytosolic Ca2+ concentration ([Ca2+]Cyt) oscillations. A mathematical compartmental closed-cell model of Ca2+ dynamics was developed that accounts for ER-mitochondria Ca2+ microdomains as the µd compartment (besides the cytosol, ER and mitochondria), Ca2+ influx to/efflux from each compartment and Ca2+ buffering. Varying the distribution of functional receptors in MAMs vs. the rest of ER/mitochondrial membranes, a parameter called the channel connectivity coefficient (to the µd), allowed for generation of [Ca2+]Cytoscillations driven by distinct mechanisms at various levels of IP3 stimulation. Oscillations could be initiated by the transient opening of IP3 receptors facing either the cytosol or the µd, and subsequent refilling of the respective compartment by Ca2+ efflux from the ER and/or the mitochondria. Only under conditions where the µd became the oscillation-driving compartment, silencing the Mitochondrial Ca2+ Uniporter led to oscillation inhibition. Thus, the model predicts that alternative mechanisms can yield [Ca2+]Cyt oscillations in non-excitable cells, and, under certain conditions, the ER-mitochondria µd can play a regulatory role.

Published
2019

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