Tobacco Smoke Constituents Trigger Cytoplasmic Calcium Release

Sassano, Maria F.; Ghosh, Arunava; Tarran, Robert

doi:10.1089/aivt.2016.0039

Cited by 14 publications

(18 citation statements)

References 29 publications

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“…These results suggest that combustion-related toxicants may play a role in the mobilization of [Ca 2+ ] i when compared with smokeless tobacco products in the HL60 leukemia cell line. In line with our findings, Sassano et al (2017) assessed the impact of 13 individual tobacco smoke constituents on [Ca 2+ ] i in HEK293T cells and found that 1-aminonaphthalene, formaldehyde, and nicotine-derived nitrosamine ketone (NNK) were able to elicit [Ca 2+ ] i increases [48].…”

Section: Discussionsupporting

confidence: 88%

“…Cytosolic Ca 2+ is a key second messenger that regulates several functions including cell growth/cell division, apoptosis, and the secretion of both ions and macromolecules [48, 50–53]. Calcium signals in cells of the immune system regulate cell differentiation, gene transcription, and effector functions crucial for the physiological functioning of the immune responses.…”

Section: Discussionmentioning

confidence: 99%

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Combustible Cigarette and Smokeless Tobacco Product Preparations Differentially Regulate Intracellular Calcium Mobilization in HL60 Cells

Arimilli¹,

Makena

Prasad

2019

Inflammation

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Changes in the level of intracellular calcium ([Ca 2+ ] i ) are central to leukocyte signaling and immune response. Although evidence suggests that cigarette smoking affects inflammatory response via an increase in intracellular calcium, it remains unclear if the use of smokeless tobacco ( e.g. , moist snuff) elicits a similar response. In this study, we evaluated the effects of tobacco product preparations (TPPs), including total particulate matter (TPM) from 3R4F reference cigarettes, smokeless tobacco extract (STE) from 2S3 reference moist snuff, and nicotine alone on Ca 2+ mobilization in HL60 cells. Treatment with TPM, but not STE or nicotine alone, significantly increased [Ca 2+ ] i in a concentration-dependent manner in HL60 cells. Moreover, TPM-induced [Ca 2+ ] i increase was not related to extracellular Ca 2+ and did not require the activation of the IP3 pathway nor involved the transient receptor potential (TRP) channels. Our findings indicate that, in cells having either intact or depleted endoplasmic reticulum (ER) Ca 2+ stores, TPM-mediated [Ca 2+ ] i increase involves cytosolic Ca 2+ pools other than thapsigargin-sensitive ER Ca 2+ stores. These results, for the first time, demonstrate that TPM triggers [Ca 2+ ] i increases, while significantly higher nicotine equivalent doses of STE or nicotine alone, did not affect [Ca 2+ ] i under the experimental conditions. In summary, our study suggests that in contrast with STE or nicotine preparations, TPM activates Ca 2+ signaling pathways in HL60 cells. The differential effect of combustible and non-combustible TPPs on Ca 2+ mobilization could be a useful in vitro endpoint for tobacco product evaluation.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Combustible Cigarette and Smokeless Tobacco Product Preparations Differentially Regulate Intracellular Calcium Mobilization in HL60 Cells

Arimilli¹,

Makena

Prasad

2019

Inflammation

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“…However, the researchers used CSE which captures a different phase of smoke than our preparation. Nevertheless, we have recently linked various components of CS, such as nicotine, to an increase in cytosolic Ca 2+ [56]. Indeed, alterations in nicotinic acetylcholine receptor activation linked to CS have been linked to CFTR dysfunction [57].…”

Section: Discussionmentioning

confidence: 99%

Increases in cytosolic Ca2+ induce dynamin- and calcineurin-dependent internalisation of CFTR

Patel

Moore

Sassano

et al. 2018

Cell. Mol. Life Sci.

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The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-regulated, apical anion channel that regulates ion and fluid transport in many epithelia including the airways. We have previously shown that cigarette smoke (CS) exposure to airway epithelia causes a reduction in plasma membrane CFTR expression which correlated with a decrease in airway surface hydration. The effect of CS on CFTR was dependent on an increase in cytosolic Ca 2+ . However, the underlying mechanism for this Ca 2+ -dependent, internalisation of CFTR is unknown. To gain a better understanding of the effect of Ca 2+ on CFTR, we performed whole cell current recordings to study the temporal effect of raising cytosolic Ca 2+ on CFTR function. We show that an increase in cytosolic Ca 2+ induced a time-dependent reduction in whole cell CFTR conductance, which was paralleled by a loss of cell surface CFTR expression, as measured by confocal and widefield fluorescence microscopy. The decrease in CFTR conductance and cell surface expression were both dynamin-dependent. Single channel reconstitution studies showed that raising cytosolic Ca 2+ per se had no direct effect on CFTR. In fact, the loss of CFTR plasma membrane activity correlated with activation of calcineurin, a Ca 2+ -dependent phosphatase, suggesting that dephosphorylation of CFTR was linked to the loss of surface expression. In support of this, the calcineurin inhibitor, cyclosporin A, prevented the Ca 2+ -induced decrease in cell surface CFTR. These results provide a hitherto unrecognised role for cytosolic Ca 2+ in modulating the residency of CFTR at the plasma membrane through a dynamin- and calcineurin-dependent mechanism. Electronic supplementary material The online version of this article (10.1007/s00018-018-2989-3) contains supplementary material, which is available to authorized users.

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“…Of note, mannitol was included as a control for potential increases in osmotic stress caused by PG/VG, but no effect on NE levels was observed. The increase in NE was subsequently shown to be associated with a rise in cytosolic calcium levels in response to nicotine; earlier studies by the same group found increases in intracellular Ca 2+ in HEK293T cells exposed to cigarette smoke, and the tobacco smoke metabolites 1-NH 2 -naphthalene, formaldehyde, nicotine, and nicotine-derived nitrosamine ketone (14).…”

mentioning

confidence: 97%

Promotion of a Protease–Antiprotease Imbalance in the Airways through Chronic Vaping

Martin¹,

Reihill²

2019

Am J Respir Crit Care Med

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Tobacco Smoke Constituents Trigger Cytoplasmic Calcium Release

Cited by 14 publications

References 29 publications

Combustible Cigarette and Smokeless Tobacco Product Preparations Differentially Regulate Intracellular Calcium Mobilization in HL60 Cells

Combustible Cigarette and Smokeless Tobacco Product Preparations Differentially Regulate Intracellular Calcium Mobilization in HL60 Cells

Increases in cytosolic Ca2+ induce dynamin- and calcineurin-dependent internalisation of CFTR

Promotion of a Protease–Antiprotease Imbalance in the Airways through Chronic Vaping

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