Air bubble contact with endothelial cells in vitro induces calcium influx and IP3-dependent release of calcium stores

Sobolewski, Peter; Kandel, Judith; Klinger, Alexandra L.; Eckmann, David M.

doi:10.1152/ajpcell.00046.2011

Cited by 40 publications

(51 citation statements)

References 45 publications

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“…Concentrations of these inhibitors were chosen based on their abilities to significantly reduce, but not completely, histamine-induced calcium responses. Higher concentrations or longer exposure induced cytotoxicity during preincubation time as also observed by Sobolewski and colleagues (35). The inactive U-73122 analog, U-73343, was purchased from Enzo Life Sciences (Farmingdale, NY) and used at same final concentration.…”

Section: Methodsmentioning

confidence: 61%

“…The existence of an equivalent delay in calcium response can also be observed with a reduction of shear magnitude, and an activation threshold of the applied shear stress was suggested (2). In a model of mechanical forces applied by micropipettes on isolated ECs, the calcium response also reaches a maximum within 10 -20 s and was further delayed by used of membrane calcium channel blockers (35). Overall, these data and ours strongly suggest that mechanically induced calcium responses require a threshold for activation and that any reduction in mechanical cue or treatment aiming at reducing accumulation of a second messenger only delays the threshold required for the calcium response.…”

Section: Discussionmentioning

confidence: 98%

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Gα_q/11-mediated intracellular calcium responses to retrograde flow in endothelial cells

Melchior

Frangos

2012

American Journal of Physiology-Cell Physiology

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Disturbed flow patterns, including reversal in flow direction, are key factors in the development of dysfunctional endothelial cells (ECs) and atherosclerotic lesions. An almost immediate response of ECs to fluid shear stress is the increase in cytosolic calcium concentration ([Ca(2+)](i)). Whether the source of [Ca(2+)](i) is extracellular, released from Ca(2+) intracellular stores, or both is still undefined, though it is likely dependent on the nature of forces involved. We have previously shown that a change in flow direction (retrograde flow) on a flow-adapted endothelial monolayer induces the remodeling of the cell-cell junction along with a dramatic [Ca(2+)](i) burst compared with cells exposed to unidirectional or orthograde flow. The heterotrimeric G protein-α q and 11 subunit (Gα(q/11)) is a likely candidate in effecting shear-induced increases in [Ca(2+)](i) since its expression is enriched at the junction and has been previously shown to be activated within seconds after onset of flow. In flow-adapted human ECs, we have investigated to what extent the Gα(q/11) pathway mediates calcium dynamics after reversal in flow direction. We observed that the elapsed time to peak [Ca(2+)](i) response to a 10 dyn/cm(2) retrograde shear stress was increased by 11 s in cells silenced with small interfering RNA directed against Gα(q/11). A similar lag in [Ca(2+)](i) transient was observed after cells were treated with the phospholipase C (PLC)-βγ inhibitor, U-73122, or the phosphatidylinositol-specific PLC inhibitor, edelfosine, compared with controls. Lower levels of inositol 1,4,5-trisphosphate accumulation seconds after the onset of flow correlated with the increased lag in [Ca(2+)](i) responses observed with the different treatments. In addition, inhibition of the inositol 1,4,5-trisphosphate receptor entirely abrogated flow-induced [Ca(2+)](i). Taken together, our results identify the Gα(q/11)-PLC pathway as the initial trigger for retrograde flow-induced endoplasmic reticulum calcium store release, thereby offering a novel approach to regulating EC dysfunctions in regions subjected to the reversal of blood flow.

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Section: Methodsmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 98%

Gα_q/11-mediated intracellular calcium responses to retrograde flow in endothelial cells

Melchior

Frangos

2012

American Journal of Physiology-Cell Physiology

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“…In addition to an increase in endothelial layer permeability, several other bioeffects have also been reported by others, such as a rise in intracellular calcium ions [9], [10], [ca 2+ ] i , and reactive oxygen species (ros) formation [11]. Interestingly, all of these responses have also been reported in endothelial cells following mechanotransduction [6], [12]- [14]. because mechanotransduction can lead to an increase in [ca 2+ ] i and/or ros, and subsequently to an increase in endothelial layer permeability, we determined whether this was also involved in microbubble-mediated increases in endothelial layer permeability.…”

mentioning

confidence: 78%

Role of intracellular calcium and reactive oxygen species in microbubble-mediated alterations of endothelial layer permeability

Kooiman

Steen

Jong

2013

IEEE Trans. Ultrason., Ferroelect., Freq. Contr.

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Drugs will be delivered to diseased tissue more efficiently if the vascular endothelial permeability is increased. Ultrasound in combination with an ultrasound contrast agent is known to increase the permeability of the endothelial layer, but the mechanism is not known. The goal of this study was to elucidate whether intracellular calcium ions, [Ca(2+)]i, and reactive oxygen species (ROS) are part of the mechanism that leads to an increased endothelial layer permeability following ultrasound and microbubble treatment. Human umbilical vein endothelial cells (HUVECs) treated for 2 min with ultrasound-activated microbubbles (1 MHz, 210 kPa, 10 000 cycles, 20 Hz repetition rate) had an increased permeability that lasted up to 12 h. Recovery of permeability after 2 h was only found when HUVECs were preincubated with the [Ca(2+)]i chelator BAPTA-AM or the antioxidant butylated hydroxytoluene (BHT). This suggests that both [Ca(2+)]i and ROS play an important role in the mechanism of increased permeability following ultrasound in combination with microbubble treatment.

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“…Previously, it has been shown that cells respond in conventional and in inverted interface experiments with intracellular Ca 2ϩ signals (55,56,63). Here we extended those studies using agonists and inhibitors for various channels and pathways (Fig.…”

Section: Conventional Interface Experiments Seementioning

confidence: 99%

Interfacial stress affects rat alveolar type II cell signaling and gene expression

Hobi

Ravasio

Haller

2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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.) showed that contact of alveolar epithelial type II cells with an air-liquid interface (I AL) leads to a paradoxical situation. It is a potential threat that can cause cell injury, but also a Ca 2ϩ -dependent stimulus for surfactant secretion. Both events can be explained by the impact of interfacial tensile forces on cellular structures. Here, the strength of this mechanical stimulus became also apparent in microarray studies by a rapid and significant change on the transcriptional level. Cells challenged with an IAL in two different ways showed activation/inactivation of cellular pathways involved in stress response and defense, and a detailed Pubmatrix search identified genes associated with several lung diseases and injuries. Altogether, they suggest a close relationship of interfacial stress sensation with current models in alveolar micromechanics. Further similarities between IAL and cell stretch were found with respect to the underlying signaling events. The source of Ca 2ϩ was extracellular, and the transmembrane Ca 2ϩ entry pathway suggests the involvement of a mechanosensitive channel. We conclude that alveolar type II cells, due to their location and morphology, are specific sensors of the IAL, but largely protected from interfacial stress by surfactant release. cell deformation; cell injury; mechanotransduction; microarray; stretch IN THE ALVEOLI, MECHANICAL forces are a constant modulator of tissue geometry and function (4). These forces arise from multiple sources, such as cyclic stretching and compression during respiration, changes in transcapillary pressure, or surface tension at the air-liquid interface (I AL ) (22). They are probably nonuniform in space and time (26,51,67) and impose either physiological responses of the cells, or pathological ones, depending on the type of tissue or the magnitude or abnormality of forces that are at work (reviewed in Refs. 18,66,69,72). In particular, tissue stretch (ϭ tensile strain) has already been shown to be an important determinant of surfactant secretion in alveolar type II (AT II) cells (2,15,36,47,71,73). Studies on single cells revealed that stretch induces an elevation of the intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) (23, 73), perhaps via mechanosensitive ion channels like the wellcharacterized transient receptor potential (TRP) vanilloids (reviewed in Refs. 16,77). Recently, the panoply of mechanosensitive mechanisms was expanded by the finding that the I AL , the "normal" microenvironment of the AT II cells (6), may be a strong mechanical incentive as well. Two recent independent studies (55, 56) described a stimulating, but also harmful, effect of an I AL on the AT II cell function. Interestingly, interfacial contact is followed by an increase in [Ca 2ϩ ] i and release of ATP, both of which stimulate secretion (reviewed in Refs. 1, 44, 59). It has even been speculated that this response could act within a feedback loop to continuously monitor and to adjust the physical properties of the interface or the hypophase below.In addition...

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Air bubble contact with endothelial cells in vitro induces calcium influx and IP3-dependent release of calcium stores

Cited by 40 publications

References 45 publications

Gα_q/11-mediated intracellular calcium responses to retrograde flow in endothelial cells

Gα_q/11-mediated intracellular calcium responses to retrograde flow in endothelial cells

Role of intracellular calcium and reactive oxygen species in microbubble-mediated alterations of endothelial layer permeability

Interfacial stress affects rat alveolar type II cell signaling and gene expression

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Air bubble contact with endothelial cells in vitro induces calcium influx and IP3-dependent release of calcium stores

Cited by 40 publications

References 45 publications

Gαq/11-mediated intracellular calcium responses to retrograde flow in endothelial cells

Gαq/11-mediated intracellular calcium responses to retrograde flow in endothelial cells

Role of intracellular calcium and reactive oxygen species in microbubble-mediated alterations of endothelial layer permeability

Interfacial stress affects rat alveolar type II cell signaling and gene expression

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Gα_q/11-mediated intracellular calcium responses to retrograde flow in endothelial cells

Gα_q/11-mediated intracellular calcium responses to retrograde flow in endothelial cells