Modulation of cardiac mechanosensitive ion channels involves superoxide, nitric oxide and peroxynitrite

Dyachenko, V. V.; Rueckschloss, Uwe; Isenberg, Gerrit

doi:10.1016/j.ceca.2008.06.002

Cited by 32 publications

(28 citation statements)

References 45 publications

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“…This dependence on PI3K was also observed in another independent study (113). Whether PI3K is activated by oxidant radicals produced by NADPH oxidase (following AT1R stimulation by autocrine/paracrine production of angiotensin II), as proposed for other stretch-activated channels (52), remains an open question.…”

Section: Autocrine Production Of No By Mechanical Forces: Activation mentioning

confidence: 72%

“…The production of NO from single, isolated cardiomyocytes in response to stretch was also demonstrated using the NO-sensitive fluorescent dye DAF2. Notably, another independent study using specific NOSdeficient cells confirmed the involvement of eNOS (but not nNOS) as the mechanosensitive isoform responsible for NO production by single cardiac myocytes in response to stretch (113).…”

Section: Autocrine Production Of No By Mechanical Forces: Activation mentioning

confidence: 80%

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eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

Balligand¹,

Feron²,

Dessy³

2009

Physiological Reviews

391

328

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Nitric oxide production in response to flow-dependent shear forces applied on the surface of endothelial cells is a fundamental mechanism of regulation of vascular tone, peripheral resistance, and tissue perfusion. This implicates the concerted action of multiple upstream "mechanosensing" molecules reversibly assembled in signalosomes recruiting endothelial nitric oxide synthase (eNOS) in specific subcellular locales, e.g., plasmalemmal caveolae. Subsequent short- and long-term increases in activity and expression of eNOS translate this mechanical stimulus into enhanced NO production and bioactivity through a complex transcriptional and posttranslational regulation of the enzyme, including by shear-stress responsive transcription factors, oxidant stress-dependent regulation of transcript stability, eNOS regulatory phosphorylations, and protein-protein interactions. Notably, eNOS expressed in cardiac myocytes is amenable to a similar regulation in response to stretching of cardiac muscle cells and in part mediates the length-dependent increase in cardiac contraction force. In addition to short-term regulation of contractile tone, eNOS mediates key aspects of cardiac and vascular remodeling, e.g., by orchestrating the mobilization, recruitment, migration, and differentiation of cardiac and vascular progenitor cells, in part by regulating the stabilization and transcriptional activity of hypoxia inducible factor in normoxia and hypoxia. The continuum of the influence of eNOS in cardiovascular biology explains its growing implication in mechanosensitive aspects of integrated physiology, such as the control of blood pressure variability or the modulation of cardiac remodeling in situations of hemodynamic overload.

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Section: Autocrine Production Of No By Mechanical Forces: Activation mentioning

confidence: 72%

Section: Autocrine Production Of No By Mechanical Forces: Activation mentioning

confidence: 80%

eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

Balligand¹,

Feron²,

Dessy³

2009

Physiological Reviews

391

328

View full text Add to dashboard Cite

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“…There is convincing evidence that activation of stretch-activated calcium channels is linked to stimulation of endothelial nitric oxide synthase and rapid generation of NO and ONOO − . 43 The kinetics of the penetration of the cell membrane by silica nanoparticles most likely involves a flux of calcium ions into the cytoplasm. 44 Therefore, silica nanoparticles are likely to stimulate calcium-dependent NO release in endothelial cells.…”

mentioning

confidence: 99%

Amorphous silica nanoparticles trigger nitric oxide/peroxynitrite imbalance in human endothelial cells: inflammatory and cytotoxic effects

Medina¹,

Jacoby²,

Malinski³

et al. 2011

IJN

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Background The purpose of this study was to investigate the mechanism of noxious effects of amorphous silica nanoparticles on human endothelial cells. Methods Nanoparticle uptake was examined by transmission electron microscopy. Electrochemical nanosensors were used to measure the nitric oxide (NO) and peroxynitrite (ONOO − ) released by a single cell upon nanoparticle stimulation. The downstream inflammatory effects were measured by an enzyme-linked immunosorbent assay, real-time quantitative polymerase chain reaction, and flow cytometry, and cytotoxicity was measured by lactate dehydrogenase assay. Results We found that the silica nanoparticles penetrated the plasma membrane and rapidly stimulated release of cytoprotective NO and, to a greater extent, production of cytotoxic ONOO − . The low [NO]/[ONOO − ] ratio indicated increased nitroxidative/oxidative stress and correlated closely with endothelial inflammation and necrosis. This imbalance was associated with nuclear factor κB activation, upregulation of key inflammatory factors, and cell death. These effects were observed in a nanoparticle size-dependent and concentration-dependent manner. Conclusion The [NO]/[ONOO − ] imbalance induced by amorphous silica nanoparticles indicates a potentially deleterious effect of silica nanoparticles on vascular endothelium.

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“…In a recent study, the same group demonstrated that mechanical deformation of murine ventricular myocytes activates TRPC6 channels, together with reducing Kir2.3 channel activity, on the basis that the tarantula peptide GsMTx-4 and the antibody Ab-TRPC6 prevented current activation [56]. Furthermore, the authors proposed that the signaling cascade involves activation by integrins of the AT1 receptors, which trigger the production of nitric oxide and superoxide via NOS3 and NAD(P)H oxidase, respectively, to form peroxynitrite that stimulates the activity of phospholipases [57]. Compelling evidence have been provided to show that AT1 receptors demonstrate a conformational switch upon mechanical activation while the tight binding of candesartan to the AT1 receptors stabilizes them in their inactive conformation [58].…”

Section: Mechanosensitive Trp Channelsmentioning

confidence: 97%

TRP Channels in Cardiac Arrhythmia: Their Role During Purinergic Activation Induced by Ischemia

Vassort¹,

Álvarez²

2011

Heart Rate and Rhythm

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Modulation of cardiac mechanosensitive ion channels involves superoxide, nitric oxide and peroxynitrite

Cited by 32 publications

References 45 publications

eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

Amorphous silica nanoparticles trigger nitric oxide/peroxynitrite imbalance in human endothelial cells: inflammatory and cytotoxic effects

TRP Channels in Cardiac Arrhythmia: Their Role During Purinergic Activation Induced by Ischemia

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