Presentation Details
| Ace2 is Endogenously Expressed in Taste Buds and its Conditional Deletion From the Lingual Epithelium Results in Enhanced Neural Responses Emma Heisey1, Guangkuo Dong2, Yonggang Bao1, Hongyan Xu3, Lin Gan1, Lynnette McCluskey1. 1Department of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA.2Department of Cell Biology and Physiology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.3School of Public Health, Department of Biostatistics, Data Science and Epidemiology Medical College of Georgia, Augusta University, Augusta, GA, USA |
Abstract
Angiotensin converting enzyme 2 (Ace2) is the primary receptor used by severe acute respiratory syndrome coronavirus 2 (Sars-CoV-2) to enter host cells, leading to loss of taste, smell, and chemethesis by unknown mechanisms. Following viral entry, Ace2 is downregulated, disrupting the renin-angiotensin-aldosterone system (RAAS). Ace2 stabilizes RAAS to reduce inflammation and maintain homeostasis. While Ace2 is well characterized in other systems, its expression and biological role in the taste system remains unclear. To study this, we developed two mouse strains: a tamoxifen-inducible reporter to visualize endogenous Ace2 expression (Ace2CE/+:Rosa26-tdTomato) and a conditional knockout (Ace2fl/fl:K14-Cre,“Ace2 cKO”) that deletes Ace2 from taste buds and surrounding epithelium. Preliminary data show robust Ace2 mRNA expression in circumvallate and anterior taste buds of wild type mice. Reporter mice reveal Ace2 expression in keratin 8 (K8)+ taste buds, including type III taste receptor cells (TRCs) compared to corn oil controls. Neurophysiological recordings from the chorda tympani nerve revealed that male Ace2 cKO mice had enhanced sweet and bitter responses while both sexes had increased responses to the sour stimulus, citric acid. The spatial distribution and composition of taste buds was altered in parallel with functional changes. Male Ace2 cKO had an increase of type II TRCs, fewer type III TRCs, and taste buds were more closely spaced in the rear of the fungiform field. These results indicate that Ace2 is endogenously expressed in taste buds and TRCs and conditional deletion alters taste bud patterning and cell composition resulting in enhanced neural responses. Ongoing studies aim to identify additional Ace2 expressing cell types and transcriptional changes underlying functional effects.
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