Hyperosmotic stress promotes endoplasmic reticulum stress-dependent apoptosis in adult rat cardiac myocytes

Burgos, Juan Ignacio; Morell, Malena; Mariángelo, Juan Ignacio Elio; Petroff, Martín Gerardo Vila

doi:10.1007/s10495-019-01558-4

Cited by 26 publications

(25 citation statements)

References 86 publications

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“…Second, persistent hyperosmotic shrinkage also causes apoptosis (Bortner and Cidlowski, 1996;Horio et al, 2001;Friis et al, 2005;Maeno et al, 2006a,b;Burgos et al, 2019;Michea et al, 2000;Luo et al, 2007;Ernest et al, 2008;Shimizu et al, 2007). Many cell types, when exposed to hyperosmotic solutions, gradually restore their volume through a process known as regulatory volume increase (RVI).…”

Section: Introductionmentioning

confidence: 99%

Evidence for macromolecular crowding as a direct apoptotic stimulus

Rana

Kurokawa

Model

2020

Journal of Cell Science

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Potassium loss and persistent shrinkage have both been implicated in apoptosis but their relationship and respective roles remain controversial. We approached this problem by clamping intracellular sodium and potassium in HeLa or MDCK cells using a combination of ionophores. Although ionophore treatment caused significant cell swelling, the initial volume could be restored and further reduced by application of sucrose. The swollen cells treated with ionophores remained viable for at least 8 h without any signs of apoptosis. Application of sucrose and the resulting shrinkage caused volumedependent intrinsic apoptosis with all its classical features: inversion of phosphatidylserine, caspase activation and Bcl-2-dependent release of cytochrome c from mitochondria. In other experiments, apoptosis was induced by addition of the protein kinase inhibitor staurosporine at various degrees of swelling. Our results show that: (1) persistent shrinkage can cause apoptosis regardless of intracellular sodium or potassium composition or of the state of actin cytoskeleton; (2) strong potassium dependence of caspase activation is only observed in swollen cells with a reduced density of cytosolic proteins. We conclude that macromolecular crowding can be an important factor in determining the transition of cells to apoptosis.

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Section: Introductionmentioning

confidence: 99%

Evidence for macromolecular crowding as a direct apoptotic stimulus

Rana

Kurokawa

Model

2020

Journal of Cell Science

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“…In addition, similar to most number of studied cells (Matthews and Feldman, 1996;Dmitrieva et al, 2001;Terada et al, 2001;Galvez et al, 2003;Reinehr and Häussinger, 2006;Png et al, 2011;Clouzeau et al, 2012;Burgos et al, 2019), significant shrinkage in hyperosmotic solutions is enough to trigger apoptosis of RVSMC (Orlov et al, 2004a). Because cell volume regulation is mediated by monovalent cations transmembrane gradient (Mongin and Orlov, 2001;Bortner and Cidlowski, 2007;Hoffmann et al, 2009; Pasantes-Morales, 2016; Delpire and Gagnon, 2018), we exposed cells to CTS.…”

Section: Ouabain Protects Rodent Cells From Apoptosis Via Expression mentioning

confidence: 89%

Ouabain-Induced Cell Death and Survival. Role of α1-Na,K-ATPase-Mediated Signaling and [Na+]i/[K+]i-Dependent Gene Expression

et al. 2020

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Ouabain is of cardiotonic steroids (CTS) family that is plant-derived compounds and is known for many years as therapeutic and cytotoxic agents. They are specific inhibitors of Na,K-ATPase, the enzyme, which pumps Na + and K + across plasma membrane of animal cells. Treatment of cells by CTS affects various cellular functions connected with the maintenance of the transmembrane gradient of Na + and K +. Numerous studies demonstrated that binding of CTS to Na,K-ATPase not only suppresses its activity but also induces some signal pathways. This review is focused on different mechanisms of two ouabain effects: their ability (1) to protect rodent cells from apoptosis through the expression of [Na + ] i-sensitive genes and (2) to trigger death of non-rodents cells (so-called «oncosis»), possessing combined markers of «classic» necrosis and «classic» apoptosis. Detailed study of oncosis demonstrated that the elevation of the [Na + ] i /[K + ] i ratio is not a sufficient for its triggering. Non-rodent cell death is determined by the characteristic property of "sensitive" to ouabain α1-subunit of Na,K-ATPase. In this case, ouabain binding leads to enzyme conformational changes triggering the activation of p38 mitogen-activated protein kinases (MAPK) signaling. The survival of rodent cells with ouabain-«resistant» α1-subunit is connected with another conformational transition induced by ouabain binding that results in the activation of ERK 1/2 signaling pathway.

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“…Disorders in plasma osmolality may induce/intensify cardiac failure per se. Experimental models have documented that hyperosmotic stress can promote endoplasmic reticulum stress via increases in the cardiac myocyte calcium content, also a trigger for myocyte apoptosis and hyperglycemia-induced myocyte death [15]. Additionally, an increase in extracellular osmolarity impairs cardiac contraction following disorders in the intracellular calcium homeostasis [30].…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, raised plasma osmolality has shown to be an important risk factor for poor outcome in patients with heart failure [13,15,16,31]. Some authors have documented that the increase in plasma osmolality above 310 mOsm kg/H 2 O significantly increases the necessity for use of vasoactive drugs and the risk of death [16,31].…”

Section: Discussionmentioning

confidence: 99%

“…An increase in plasma osmolality as well as osmolal gap may lead to organ damage. For example, hyperosmolality can cause acute kidney injury (AKI) [11,12], and also impair cardiac function, increasing mortality in patients with heart failure [13][14][15]. In fact, hyperosmotic stress promotes cardiomyocyte injury [16], and an increase in plasma osmolality following hyperosmolar contrast administration can cause significant disorders in cardiac repolarisation reflected in electrocardiographic measurement [17,18].…”

Section: Introductionmentioning

confidence: 99%

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Plasma Hyperosmolality Prolongs QTc Interval and Increases Risk for Atrial Fibrillation in Traumatic Brain Injury Patients

Dąbrowski

Siwicka-Gieroba

Robba

et al. 2020

JCM

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Introduction: Hyperosmotic therapy with mannitol is frequently used for treatment cerebral edema, and 320 mOsm/kg H2O has been recommended as a high limit for therapeutic plasma osmolality. However, plasma hyperosmolality may impair cardiac function, increasing the risk of cardiac events. The aim of this study was to analyze the relation between changes in plasma osmolality and electrocardiographic variables and cardiac arrhythmia in patients treated for isolated traumatic brain injury (iTBI). Methods: Adult iTBI patients requiring mannitol infusion following cerebral edema, and with a Glasgow Coma Score below 8, were included. Plasma osmolality was measured with Osmometr 800 CLG. Spatial QRS-T angle (spQRS-T), corrected QT interval (QTc) and STJ segment were calculated from digital resting 12-lead ECGs and analyzed in relation to four levels of plasma osmolality: (A) <280 mOsm/kg H2O; (B) 280–295 mOsm/kg H2O; (C) 295–310 mOsm/kg H2O; and (D) >310 mOsm/kg H2O. All parameters were measured during five consecutive days of treatment. Results: 94 patients aged 18-64 were studied. Increased plasma osmolality correlated with prolonged QTc (p < 0.001), intensified disorders in STJ and increased the risk for cardiac arrhythmia. Moreover, plasma osmolality >313 mOms/kg H2O significantly increased the risk of QTc prolongation >500 ms. Conclusion: In patients treated for iTBI, excessively increased plasma osmolality contributes to electrocardiographic disorders including prolonged QTc, while also correlating with increased risk for cardiac arrhythmias.

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Hyperosmotic stress promotes endoplasmic reticulum stress-dependent apoptosis in adult rat cardiac myocytes

Cited by 26 publications

References 86 publications

Evidence for macromolecular crowding as a direct apoptotic stimulus

Evidence for macromolecular crowding as a direct apoptotic stimulus

Ouabain-Induced Cell Death and Survival. Role of α1-Na,K-ATPase-Mediated Signaling and [Na+]i/[K+]i-Dependent Gene Expression

Plasma Hyperosmolality Prolongs QTc Interval and Increases Risk for Atrial Fibrillation in Traumatic Brain Injury Patients

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