RND3 Potentiates Proinflammatory Activation through NOTCH Signaling in Activated Macrophages

Macrophage activation is a complex process with multiple control elements that ensures an adequate response to the aggressor pathogens and, on the other hand, avoids an excess of inflammatory activity that could cause tissue damage. In this study, we have identified RND3, a small GTP-binding protein...

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Main Authors: María José Romero de Ávila, Susana López-López, Aarón García-Blázquez, Almudena Ruiz-García, María Julia González-Gómez, María Luisa Nueda, Victoriano Baladrón, Ignacio Pérez-Roger, Enric Poch, Begoña Ballester-Lurbe, José Javier García-Ramírez, Eva M. Monsalve, María José M. Díaz-Guerra
Format: Article
Language:English
Published: Wiley 2024-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2024/2264799
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author María José Romero de Ávila
Susana López-López
Aarón García-Blázquez
Almudena Ruiz-García
María Julia González-Gómez
María Luisa Nueda
Victoriano Baladrón
Ignacio Pérez-Roger
Enric Poch
Begoña Ballester-Lurbe
José Javier García-Ramírez
Eva M. Monsalve
María José M. Díaz-Guerra
author_facet María José Romero de Ávila
Susana López-López
Aarón García-Blázquez
Almudena Ruiz-García
María Julia González-Gómez
María Luisa Nueda
Victoriano Baladrón
Ignacio Pérez-Roger
Enric Poch
Begoña Ballester-Lurbe
José Javier García-Ramírez
Eva M. Monsalve
María José M. Díaz-Guerra
author_sort María José Romero de Ávila
collection DOAJ
description Macrophage activation is a complex process with multiple control elements that ensures an adequate response to the aggressor pathogens and, on the other hand, avoids an excess of inflammatory activity that could cause tissue damage. In this study, we have identified RND3, a small GTP-binding protein, as a new element in the complex signaling process that leads to macrophage activation. We show that RND3 expression is transiently induced in macrophages activated through Toll receptors and potentiated by IFN-γ. We also demonstrate that RND3 increases NOTCH signaling in macrophages by favoring NOTCH1 expression and its nuclear activity; however, Rnd3 expression seems to be inhibited by NOTCH signaling, setting up a negative regulatory feedback loop. Moreover, increased RND3 protein levels seem to potentiate NFκB and STAT1 transcriptional activity resulting in increased expression of proinflammatory genes, such as Tnf-α, Irf-1, or Cxcl-10. Altogether, our results indicate that RND3 seems to be a new regulatory element which could control the activation of macrophages, able to fine tune the inflammatory response through NOTCH.
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issn 2314-7156
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publishDate 2024-01-01
publisher Wiley
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series Journal of Immunology Research
spelling doaj-art-dd2c93a234c849d8a88d5e6ba21286a82025-08-20T02:21:33ZengWileyJournal of Immunology Research2314-71562024-01-01202410.1155/2024/2264799RND3 Potentiates Proinflammatory Activation through NOTCH Signaling in Activated MacrophagesMaría José Romero de Ávila0Susana López-López1Aarón García-Blázquez2Almudena Ruiz-García3María Julia González-Gómez4María Luisa Nueda5Victoriano Baladrón6Ignacio Pérez-Roger7Enric Poch8Begoña Ballester-Lurbe9José Javier García-Ramírez10Eva M. Monsalve11María José M. Díaz-Guerra12Medical SchoolMedical SchoolMedical SchoolBiochemistry and Molecular Biology BranchMedical SchoolBiochemistry and Molecular Biology BranchMedical SchoolDepartment of Biomedical Sciences School of Health SciencesDepartment of Biomedical Sciences School of Health SciencesDepartment of Biomedical Sciences School of Health SciencesMedical SchoolMedical SchoolMedical SchoolMacrophage activation is a complex process with multiple control elements that ensures an adequate response to the aggressor pathogens and, on the other hand, avoids an excess of inflammatory activity that could cause tissue damage. In this study, we have identified RND3, a small GTP-binding protein, as a new element in the complex signaling process that leads to macrophage activation. We show that RND3 expression is transiently induced in macrophages activated through Toll receptors and potentiated by IFN-γ. We also demonstrate that RND3 increases NOTCH signaling in macrophages by favoring NOTCH1 expression and its nuclear activity; however, Rnd3 expression seems to be inhibited by NOTCH signaling, setting up a negative regulatory feedback loop. Moreover, increased RND3 protein levels seem to potentiate NFκB and STAT1 transcriptional activity resulting in increased expression of proinflammatory genes, such as Tnf-α, Irf-1, or Cxcl-10. Altogether, our results indicate that RND3 seems to be a new regulatory element which could control the activation of macrophages, able to fine tune the inflammatory response through NOTCH.http://dx.doi.org/10.1155/2024/2264799
spellingShingle María José Romero de Ávila
Susana López-López
Aarón García-Blázquez
Almudena Ruiz-García
María Julia González-Gómez
María Luisa Nueda
Victoriano Baladrón
Ignacio Pérez-Roger
Enric Poch
Begoña Ballester-Lurbe
José Javier García-Ramírez
Eva M. Monsalve
María José M. Díaz-Guerra
RND3 Potentiates Proinflammatory Activation through NOTCH Signaling in Activated Macrophages
Journal of Immunology Research
title RND3 Potentiates Proinflammatory Activation through NOTCH Signaling in Activated Macrophages
title_full RND3 Potentiates Proinflammatory Activation through NOTCH Signaling in Activated Macrophages
title_fullStr RND3 Potentiates Proinflammatory Activation through NOTCH Signaling in Activated Macrophages
title_full_unstemmed RND3 Potentiates Proinflammatory Activation through NOTCH Signaling in Activated Macrophages
title_short RND3 Potentiates Proinflammatory Activation through NOTCH Signaling in Activated Macrophages
title_sort rnd3 potentiates proinflammatory activation through notch signaling in activated macrophages
url http://dx.doi.org/10.1155/2024/2264799
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