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Pflugers Arch. 2018 May 12. doi: 10.1007/s00424-018-2148-6. [Epub ahead of print]

TRPA1 channels: expression in non-neuronal murine lung tissues and dispensability for hyperoxia-induced alveolar epithelial hyperplasia.

Author information

1
Walther Straub Institute of Pharmacology and Toxicology, Member of the German Center for Lung Research (DZL), LMU Munich, Nußbaumstr. 26, 80336, Munich, Germany.
2
Bundeswehr Institute of Pharmacology and Toxicology, Munich, Germany.
3
Comprehensive Pneumology Center, Institute of Lung Biology and Disease, Member of the German Center for Lung Research (DZL), Helmholtz Center Munich, Munich, Germany.
4
German Center for Lung Research, Comprehensive Pneumology Center, Munich, Germany.
5
German Centre for Cardiovascular Research, Munich Heart Alliance, Munich, Germany.
6
Walther Straub Institute of Pharmacology and Toxicology, Member of the German Center for Lung Research (DZL), LMU Munich, Nußbaumstr. 26, 80336, Munich, Germany. Alexander.Dietrich@lrz.uni-muenchen.de.
7
German Center for Lung Research, Comprehensive Pneumology Center, Munich, Germany. Alexander.Dietrich@lrz.uni-muenchen.de.

Abstract

Transient receptor potential A1 (TRPA1) channels were originally characterized in neuronal tissues but also identified in lung epithelium by staining with fluorescently coupled TRPA1 antibodies. Its exact function in non-neuronal tissues, however, is elusive. TRPA1 is activated in vitro by hypoxia and hyperoxia and is therefore a promising TRP candidate for sensing hyperoxia in pulmonary epithelial cells and for inducing alveolar epithelial hyperplasia. Here, we isolated tracheal, bronchial, and alveolar epithelial cells and show low but detectable TRPA1 mRNA levels in all these cells as well as TRPA1 protein by Western blotting in alveolar type II (AT II) cells. We quantified changes in intracellular Ca2+ ([Ca2+]i) levels induced by application of hyperoxic solutions in primary tracheal epithelial, bronchial epithelial, and AT II cells isolated from wild-type (WT) and TRPA1-deficient (TRPA1-/-) mouse lungs. In all cell types, we detected hyperoxia-induced rises in [Ca2+]i levels, which were not significantly different in TRPA1-deficient cells compared to WT cells. We also tested TRPA1 function in a mouse model for hyperoxia-induced alveolar epithelial hyperplasia. A characteristic significant increase in thickening of alveolar tissues was detected in mouse lungs after exposure to hyperoxia, but not in normoxic WT and TRPA1-/- controls. Quantification of changes in lung morphology in hyperoxic WT and TRPA1-/- mice, however, again revealed no significant changes. Therefore, TRPA1 expression does neither appear to be a key player for hyperoxia-induced changes in [Ca2+]i levels in primary lung epithelial cells, nor being essential for the development of hyperoxia-induced alveolar epithelial hyperplasia.

KEYWORDS:

Alveolar epithelial hyperplasia; Human lung tissues; Hyperoxia; Murine lung tissues; TRPA1; mRNA expression

PMID:
29754249
DOI:
10.1007/s00424-018-2148-6

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