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Related Experiment Video

Updated: Jul 14, 2026

Optimal Lentivirus Production and Cell Culture Conditions Necessary to Successfully Transduce Primary Human Bronchial Epithelial Cells

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Published on: July 22, 2016

Swelling-activated K+ efflux and regulatory volume decrease efficiency in human bronchial epithelial cells.

Adrian Caplanusi¹, Kwang-Jin Kim, Els Lariviere

¹Laboratory of Physiology, K. U. Leuven, Campus Gasthuisberg, B-3000 Leuven, Belgium.

The Journal of Membrane Biology

|June 5, 2007

Summary

Cell swelling triggers potassium (K+) efflux, crucial for volume regulation in human bronchial cells. Blocking K+ channels inhibits this regulatory volume decrease (RVD) process.

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Culturing of Human Nasal Epithelial Cells at the Air Liquid Interface

Culturing of Human Nasal Epithelial Cells at the Air Liquid Interface

Published on: October 8, 2013

Area of Science:

Cell Biology
Physiology
Ion Transport

Background:

Human bronchial epithelial cells (16HBE14o(-1)) are models for studying ion transport and cell volume regulation.
Regulatory Volume Decrease (RVD) is a critical cellular process for maintaining homeostasis after swelling.
Ion channels and intracellular signaling pathways play key roles in modulating RVD.

Purpose of the Study:

To investigate the correlation between K+ efflux and RVD efficiency in 16HBE14o(-1) cells.
To identify the role of specific ion channels and signaling molecules in swelling-induced K+ transport and RVD.
To explore the impact of pharmacological agents on K+ efflux and RVD.

Main Methods:

Utilized a human bronchial epithelial cell line (16HBE14o(-1)) cultured on permeable supports.
Monitored cell height changes (T(c)) as an index of cell volume.
Measured 86Rubidium (86Rb) efflux to quantify K+ channel activity during hyposmotic shock.

Main Results:

Hyposmotic shock caused significant cell swelling followed by RVD, restoring cell volume to 94% of the isosmotic value.
Basolateral 86Rb efflux increased dramatically during hyposmotic shock, while apical efflux remained negligible.
Channel blockers (GdCl3, quinine, NPPB) and protein tyrosine kinase inhibitors (Tyrphostin 23, genistein) abolished or attenuated RVD and reduced 86Rb efflux.
NPPB completely blocked hyposmosis-induced 86Rb efflux, suggesting a link between basolateral K+ and Cl- efflux.
Forskolin stimulated RVD and increased basolateral 86Rb efflux.

Conclusions:

Basolateral K+ and Cl- extrusion are critical for efficient RVD in 16HBE14o(-1) cells following cell swelling.
Ion channel activity and intracellular signaling pathways significantly influence K+ efflux and RVD.
Targeting these pathways may offer therapeutic strategies for conditions involving bronchial epithelial cell volume dysregulation.