Biology (May 2024)

Modulator Effect of AT1 Receptor Knockdown on THP-1 Macrophage Proinflammatory Activity

  • Lourdes Nallely Acevedo-Villavicencio,
  • Carlos Enrique López-Luna,
  • Juan Castillo-Cruz,
  • Rocío Alejandra Gutiérrez-Rojas,
  • Iris Selene Paredes-González,
  • Santiago Villafaña,
  • Fengyang Huang,
  • Cruz Vargas-De-León,
  • Rodrigo Romero-Nava,
  • Karla Aidee Aguayo-Cerón

DOI
https://doi.org/10.3390/biology13060382
Journal volume & issue
Vol. 13, no. 6
p. 382

Abstract

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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. Materials and 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.

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