Effect of SARS-CoV-2 Virus S1 Protein binding to ACE2 on ENaC Regulators in Cultured Adult Human Fungiform (HBO) Taste Cells| Chapter 6 | Medical Science: Recent Advances and Applications Vol. 8

 

Early, but often prolonged, symptoms of COVID-19 infection are the loss of taste, smell, and chemesthesis. The SARS-CoV-2 spike protein contains two subunits, S1 and S2. S1 contains a receptor-binding domain, which is responsible for recognizing and binding to the ACE2 receptor, a component of renin-angiotensin-aldosterone system (RAAS). We hypothesize that S1 binding to ACE2 receptor can alter the balance between the two major RAAS pathways ACE1/Ang II/AT1R and ACE2/Ang-(1–7)/MASR1, leading to changes in ENaC expression and responses to NaCl in salt-sensing human fungiform taste cells. To test this hypothesis, we used molecular techniques to demonstrate that G-protein-coupled estrogen receptor (GPER1), transient receptor potential cation channel subfamily V member 1 (TRPV1) and components of RAAS are expressed in \(\delta\)-ENaC-positive cultured adult human fungiform (HBO) taste cells. Our results suggest that RAAS components function in a complex with ENaC and TRPV1 to modulate salt sensing and thus salt intake in humans. Our results further show that the binding of a mutated S1 protein to ACE2 decreases ACE2 expression in HBO cells.

 

Author(s) Details

Mehmet Hakan Özdener
Monell Chemical Senses Center, Philadelphia, PA 19104, USA

 

Sunila Mahavadi
Department of Biology, Center for Biomedical Research, Tuskegee University, Tuskegee, AL 36088, USA.

 

Shobha Mummalaneni
Department of Cellular, Molecular, and Genetic Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA.

 

Vijay Lyall
Department of Cellular, Molecular, and Genetic Medicine, Virginia Commonwealth University,Richmond, VA 23298, USA.

 

Please see the book here:- https://doi.org/10.9734/bpi/msraa/v8/5835

Chronic Angiotensin II (AngII) – Induced Hypertension is Attenuated by Overexpression of Copper/Zinc Superoxide Dismutase in the Median Preoptic Nucleus | Chapter 08 | New Horizons in Medicine and Medical Research Vol. 9

 Angiotensin II (AngII) can reach the brain through circumventricular organs (CVOs), such as the subfornical organ (SFO) and the organum vasculosum of the lamina terminalis, to control blood pressure (OVLT). We wanted to see if elevated amounts of superoxide in the OVLT play a role in AngII's hypertensive effects. To allow superoxide dismutase overexpression, adenoviral vectors carrying human copper/zinc superoxide dismutase (CuZnSOD) or control adenovirus (AdEmpty) were injected directly into the OVLT of rats. Rats were administered AngII (10 ng/kg/min) intravenously for ten days after three days of saline infusion. After 10 days, AdEmpty rats (n = 6) had a blood pressure rise of 33 8 mmHg, whereas rats overexpressing CuZnSOD (n = 8) in the OVLT had a blood pressure increase of just 18 5 mmHg Infusion of AngII. These findings back up the idea that excessive OVLT production plays a role in the development of persistent AngII-dependent hypertension. The brain is thought to perceive circulating angiotensin II (AngII) levels through circumventricular organs like the subfornical organ (SFO) and adjust sympathetic nervous system output accordingly. However, the cellular signalling pathways involved in these interactions remain unclear. We investigated if an underlying mechanism in the long-term hypertensive consequences of chronic AngII is overproduction of intracellular superoxide in the median preoptic nucleus (MnPO). Adenoviral vectors carrying human CuZnSOD (AdCuZnSOD) or a control vector (AdEmpty) were directly injected into the MnPO of rats equipped with aorta telemetric transmitters for arterial pressure measurement. Rats were administered AngII (10 ng/kg/min) intravenously for ten days after a three-day saline infusion control period. In the MnPO, rats overexpressing CuZnSOD (n = 7) had after ten days of AngII infusion, blood pressure increased only 6 2 mmHg, but blood pressure increased 21 4 mmHg in AdEmpty-infected rats (n = 9). These results support the idea that MnPO production contributes to the development of chronic AngII-dependent hypertension.

Author(S) Details

John P. Collister
Department of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108, USA.

Mitch Bellrichard
Department of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108, USA.

Donna Drebes
Department of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108, USA.

David Nahey
Department of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108, USA.

Jun Tian
Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.

Matthew C. Zimmerman
Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.

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