# Effect of Electronic Cigarette Vapour Exposure on Ca2+- and cAMP-Dependent Ion Transport in Human Airway Epithelial Cells

**Authors:** Ya Niu, Chung-Yin Yip, Ke-wu Pan, Judith Choi-Wo Mak, Wing-Hung Ko

PMC · DOI: 10.1007/s00408-025-00805-7 · Lung · 2025-03-18

## TL;DR

This study shows that e-cigarette vapor, like traditional cigarette smoke, impairs ion transport in human airway cells, potentially leading to lung injury.

## Contribution

The study reveals that e-cigarette vapor disrupts Ca2+ and cAMP-dependent ion transport in airway epithelial cells, similar to traditional cigarette smoke.

## Key findings

- E-vapour exposure significantly reduced agonist-induced increases in Ca2+ and cAMP signaling in human airway cells.
- E-vapour caused a decrease in electrogenic ion transport (ISC) comparable to traditional cigarette smoke.
- The observed dysfunction did not correlate with changes in ion channel or transporter protein levels.

## Abstract

The popularity of electronic cigarettes (e-cigarettes) has grown exponentially over the past few years, and teenagers now prefer them to tobacco cigarettes. We determined whether exposure to e-cigarette vapour (e-vapour) adversely affects ion transport using human airway epithelial cell lines 16HBE14o- and Calu-3 and well-differentiated primary human bronchial epithelial cells (HBEs).

We concurrently measured fluorescent signals and short-circuit current (ISC), an indicator of electrogenic ion transport, in polarised epithelia. The P2Y receptor-mediated signalling pathway was used to induce an increase in intracellular calcium concentration ([Ca2+]i) and ISC. We used a single-polypeptide fluorescence resonance energy transfer reporter based on exchange proteins directly activated by cAMP (Epac) to measure forskolin-induced changes in cAMP and ISC.

We compared the effects of e-vapour to those of traditional cigarette smoke (CS) on the human airway cell models. In all three cell types, e-vapour, similar to CS, significantly reduced agonist-induced increases in Ca2+ or cAMP signalling and ISC. However, reductions in the epithelial electrolyte transport activities did not correlate with any changes in the protein levels of various ion channels and transporters.

Our data suggest that e-vapour is not harmless and causes ion transport dysfunction similar to CS, thereby predisposing e-cigarette users to vaping-induced lung injury.

## Linked entities

- **Proteins:** RAPGEF3 (Rap guanine nucleotide exchange factor 3)
- **Chemicals:** forskolin (PubChem CID 47936)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Diseases:** lung injury (MESH:D055370), ion transport dysfunction (MESH:D007706)
- **Chemicals:** Ca2+ (-), forskolin (MESH:D005576), calcium (MESH:D002118)
- **Species:** Homo sapiens (human, species) [taxon 9606], Nicotiana tabacum (American tobacco, species) [taxon 4097]
- **Cell lines:** 16HBE14o — Homo sapiens (Human), Transformed cell line (CVCL_0112), Calu-3 — Homo sapiens (Human), Lung adenocarcinoma, Cancer cell line (CVCL_0609)

## Full text

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## Figures

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Source: https://tomesphere.com/paper/PMC11920333