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"Interaction between Angiotensin-converting enzyme 2 and serotonin during systemic inflammation"

Grant number: 20/12777-3
Support Opportunities:Scholarships in Brazil - Post-Doctorate
Effective date (Start): March 01, 2021
Effective date (End): February 29, 2024
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Luiz Guilherme de Siqueira Branco
Grantee:Patrícia Passaglia
Host Institution: Faculdade de Odontologia de Ribeirão Preto (FORP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Associated research grant:16/17681-9 - Pathophysiological changes during systemic inflammation, AP.TEM


The activation of the Angiotensin-converting enzyme 2 (ACE2), a component of the counter-regulatory axis of the Renin-Angiotensin System, has been reported as a potential target in the control of systemic inflammation. ACE2 is essential for the functioning of the intestinal transporter B(0)AT1, responsible for the absorption of tryptophan, a precursor of serotonin (5-HT). 5-HT is essential in controlling inflammation and can act directly on peripheral immune cells or even activate the neuroimmune pathway of the inflammatory reflex. During endotoxemia, a classic model for inducing systemic inflammation, there is a decrease in the expression of ACE2 and the B(0)AT1 transporter, as well as a reduction in 5-HT. However, although the importance of ACE2 activation for the synthesis of 5-HT and the importance of 5-HT in controlling inflammation are described separately, an integrated approach, comprising several aspects of this topic, still needs to be better elucidated. Still, considering that current studies report the possibility that activation of the ACE2/Angiotensin-(1-7) axis is a new pharmacological strategy for the treatment of anxiety and depression, and that recently, anti-inflammatory properties have been discussed of the treatment of patients with aceturate diminazene (DIZE), an ACE2 activator, we point out the importance of investigating the interaction between ACE2 and 5-HT for the modulation of systemic inflammation. Thus, we hypothesized that activation of ACE2, by DIZE, will attenuate systemic inflammation by increasing the expression of ACE2 coupled to the B(0)AT1 transporter, by increasing 5-HT and activating the inflammatory reflex in endotoxemic animals.

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