%0 Journal Article
%T Modulator Effect of AT1 Receptor Knockdown on THP-1 Macrophage Proinflammatory Activity.
%A Acevedo-Villavicencio LN
%A López-Luna CE
%A Castillo-Cruz J
%A Gutiérrez-Rojas RA
%A Paredes-González IS
%A Villafaña S
%A Huang F
%A Vargas-De-León C
%A Romero-Nava R
%A Aguayo-Cerón KA
%J Biology (Basel)
%V 13
%N 6
%D 2024 May 26
%M 38927262
%F 5.168
%R 10.3390/biology13060382
%X Currently, it is known that angiotensin II (AngII) induces inflammation, and an AT1R blockade has anti-inflammatory effects. The use of an AT1 receptor antagonist promotes the inhibition of the secretion of multiple proinflammatory cytokines in macrophages, as well as a decrease in the concentration of reactive oxygen species. The aim of this study was to determine the effect of AT1 receptor gene silencing on the modulation of cytokines (e.g., IL-1β, TNF-α, and IL-10) in THP-1 macrophages and the relation to the gene expression of NF-κB.
METHODS: We evaluated the gene expression of PPAR-γ in THP-1 macrophages using PMA (60 ng/mL). For the silencing, cells were incubated with the siRNA for 72 h and telmisartan (10 µM) was added to the medium for 24 h. After that, cells were incubated during 1 and 24 h, respectively, with Ang II (1 µM). The gene expression levels of AT1R, NF-κB, and cytokines (IL-1β, TNF-α, and IL-10) were measured by RT-qPCR.
RESULTS: We observed that silencing of the AT1 receptor causes a decrease in the expression of mRNA of proinflammatory cytokines (IL-1β and TNF-α), NF-κB, and PPAR-γ.
CONCLUSIONS: We conclude that AT1R gene silencing is an alternative to modulating the production of proinflammatory cytokines such as TNF-α and IL-1β via NF-κB in macrophages and having high blood pressure decrease.