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Identification of Cardiac Expression Pattern of Transient Receptor Potential Vanilloid Type 1 (TRPV1) Receptor using a Transgenic Reporter Mouse Model.

Authors
  • Hong, Juan1
  • Lisco, Amanda M2
  • Rudebush, Tara L2
  • Yu, Li2
  • Gao, Lie2
  • Kitzerow, Oliver1
  • Zucker, Irving H2
  • Wang, Han-Jun3
  • 1 Department of Anesthesiology, University of Nebraska Medical Center, NE, 68198, USA.
  • 2 Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, NE, 68198, USA.
  • 3 Department of Anesthesiology, University of Nebraska Medical Center, NE, 68198, USA; Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, NE, 68198, USA. Electronic address: [email protected]
Type
Published Article
Journal
Neuroscience letters
Publication Date
Oct 15, 2020
Volume
737
Pages
135320–135320
Identifiers
DOI: 10.1016/j.neulet.2020.135320
PMID: 32841712
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Transient receptor potential vanilloid type 1 (TRPV1) channels are structurally related, non-selective cation channels that exhibit a high permeability to calcium. Sensory nerve endings expressing TRPV1 channels play a prominent role in regulating the cardiac sympathetic afferent reflex and contribute to cardiac remodeling and dysfunction in chronic heart failure. However, the precise expression of TRPV1 channels in cardiomyocytes vs. non-cardiomyocytes remains debated. Here we utilized a tdTomato-GFP reporter mouse crossed with a mouse line expressing Cre recombinase under the control of the TRPV1 promoter to map the TRPV1 expression pattern in heart. In this model, TRPV1-negative cells express tdTomato protein (red), whereas TRPV1-positive cells express GFP protein (green). As we expected, substantial GFP expression was found in many small and medium diameter dorsal root ganglia neurons in heterozygous TRPV1-Cre +/-, tdTomato flox/flox +/- male mice, suggesting that this heterozygous model is sufficient for labeling TRPV1-positive cells. Furthermore, these results showed that GFP green staining was not detectable in cardiomyocytes. Instead, we found strong GFP green staining in cardiac blood vessels-thought to be arterioles-in the heart. We also observed strong GFP signals on PGP9.5-positive cardiac nerve endings in the epicardium. In summary, this study does not support the concept that TRPV1 channels are strongly expressed in mouse cardiomyocytes. We conclude that TRPV1 channels in mouse heart are mostly expressed on non-cardiomyocyte cells including cardiac nerve endings and vessels. These data have important implications for the modulations of cardiogenic reflexes. Copyright © 2020 Elsevier B.V. All rights reserved.

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