| Literature DB >> 32484458 |
Huan-Jun Lu1,2, Thien-Luan Nguyen1,2, Gyu-Sang Hong1, Sungmin Pak1, Hyesu Kim1, Hyungsup Kim1, Dong-Yoon Kim3, Sung-Yon Kim3, Yiming Shen4, Pan Dong Ryu4, Mi-Ock Lee2, Uhtaek Oh1.
Abstract
The baroreceptor reflex is a powerful neural feedback that regulates arterial pressure (AP). Mechanosensitive channels transduce pulsatile AP to electrical signals in baroreceptors. Here we show that tentonin 3 (TTN3/TMEM150C), a cation channel activated by mechanical strokes, is essential for detecting AP changes in the aortic arch. TTN3 was expressed in nerve terminals in the aortic arch and nodose ganglion (NG) neurons. Genetic ablation of Ttn3 induced ambient hypertension, tachycardia, AP fluctuations, and impaired baroreflex sensitivity. Chemogenetic silencing or activation of Ttn3+ neurons in the NG resulted in an increase in AP and heart rate, or vice versa. More important, overexpression of Ttn3 in the NG of Ttn3-/- mice reversed the cardiovascular changes observed in Ttn3-/- mice. We conclude that TTN3 is a molecular component contributing to the sensing of dynamic AP changes in baroreceptors.Entities:
Keywords: Ion channels; Molecular biology; Neuroscience; Vascular Biology
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Year: 2020 PMID: 32484458 PMCID: PMC7324181 DOI: 10.1172/JCI133798
Source DB: PubMed Journal: J Clin Invest ISSN: 0021-9738 Impact factor: 14.808