G-protein-coupled receptor MAS DeLETION produces a preeclampsia-like phenotype in FVB/N mice

Item Type:	Article
Title:	G-protein-coupled receptor MAS DeLETION produces a preeclampsia-like phenotype in FVB/N mice
Creators Name:	Vieira Pimentel, R.L. and Braga, J.F. and Velloso, E.P.P. and Lautner, R.Q. and Oliveira, M.L. and Todiras, M. and Alenina, N. and Bader, M. and de Sousa, F.G. and Beier, S.L. and Souza Dos Santos, R.A.
Abstract:	Background - An unbalance in the renin-angiotensin (Ang) system between the Ang II/AT1 and Ang-(1-7)/Mas axis appears to be involved in preeclampsia (PE), in which a reduction of Ang-(1-7) was observed. Here we tested whether the reduction in the activity of the Ang-(1-7)/Mas axis could be a contributing factor for the development of PE, using Mas-deficient (Mas-/-) mice. Methods and Results - Cardiovascular parameters were evaluated by telemetry before, during pregnancy and 4 days post partum in twenty weeks old Mas-/- and wildtype (WT) female mice. Mas-/- mice presented reduced arterial blood pressure at baseline (91.3 ± 0.8 in Mas-/- vs. 94.0 ± 0.9 mmHg in WT, Diastolic, p<0.05). However, after the 13th day of gestation, blood pressure in Mas-/- mice started to increase, time-dependently, and at day 19 of pregnancy, these animals presented a higher blood pressure in comparison to WT group (90.5 ± 0.7 in Mas-/- vs. 80.3 ± 3.5 mmHg in WT, Diastolic D19, p<0.0001). Moreover, pregnant Mas-/- mice presented fetal growth restriction, increase in urinary protein excretion as compared to non-pregnant Mas-/- , oliguria, increase in cytokines, endothelial dysfunction and reduced ACE, AT1R, ACE2, ET-1A and eNOS placental mRNA, similar to some of the clinical manifestations found in the development of preeclampsia. Conclusions- These results show that Mas-deletion produces a preeclampsia-like state in FVB/N mice. Key Words: Mas-deficient mice - preeclampsia - Angiotensin-(1-7) / Mas axis.
Keywords:	Mas-Deficient Mice, Preeclampsia, Angiotensin-(1-7) / Mas Axis, Animals, Mice
Source:	Clinical Science
ISSN:	0143-5221
Publisher:	Portland Press
Volume:	137
Number:	16
Page Range:	1249-1263
Date:	August 2023
Official Publication:	https://doi.org/10.1042/CS20220819
PubMed:	View item in PubMed

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