Inhibition of the NLRP3 inflammasome improves lifespan in animal murine model of Hutchinson–Gilford Progeria

Abstract Inflammation is a hallmark of aging and accelerated aging syndromes such as Hutchinson–Gilford progeria syndrome (HGPS). In this study, we present evidence of increased expression of the components of the NLRP3 inflammasome pathway in HGPS skin fibroblasts, an outcome that was associated wi...

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Main Authors: Alvaro González‐Dominguez, Raúl Montañez, Beatriz Castejón‐Vega, Jéssica Nuñez‐Vasco, Débora Lendines‐Cordero, Chun Wang, Gabriel Mbalaviele, José M Navarro‐Pando, Elísabet Alcocer‐Gómez, Mario D Cordero
Format: Article
Language:English
Published: Springer Nature 2021-08-01
Series:EMBO Molecular Medicine
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Online Access:https://doi.org/10.15252/emmm.202114012
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author Alvaro González‐Dominguez
Raúl Montañez
Beatriz Castejón‐Vega
Jéssica Nuñez‐Vasco
Débora Lendines‐Cordero
Chun Wang
Gabriel Mbalaviele
José M Navarro‐Pando
Elísabet Alcocer‐Gómez
Mario D Cordero
author_facet Alvaro González‐Dominguez
Raúl Montañez
Beatriz Castejón‐Vega
Jéssica Nuñez‐Vasco
Débora Lendines‐Cordero
Chun Wang
Gabriel Mbalaviele
José M Navarro‐Pando
Elísabet Alcocer‐Gómez
Mario D Cordero
author_sort Alvaro González‐Dominguez
collection DOAJ
description Abstract Inflammation is a hallmark of aging and accelerated aging syndromes such as Hutchinson–Gilford progeria syndrome (HGPS). In this study, we present evidence of increased expression of the components of the NLRP3 inflammasome pathway in HGPS skin fibroblasts, an outcome that was associated with morphological changes of the nuclei of the cells. Lymphoblasts from HGPS patients also showed increased basal levels of NLRP3 and caspase 1. Consistent with these results, the expression of caspase 1 and Nlrp3, but not of the other inflammasome receptors was higher in the heart and liver of Zmpste24−/− mice, which phenocopy the human disease. These data were further corroborated in LmnaG609G/G609G mice, another HGPS animal model. We also showed that pharmacological inhibition of the NLRP3 inflammasome by its selective inhibitor, MCC950, improved cellular phenotype, significantly extended the lifespan of progeroid animals, and reduced inflammasome‐dependent inflammation. These findings suggest that inhibition of the NLRP3 inflammasome is a potential therapeutic approach for the treatment of HGPS.
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spelling doaj-art-741ada3b7d4b430aadbd36423e7df82b2025-08-20T03:05:53ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842021-08-0113101710.15252/emmm.202114012Inhibition of the NLRP3 inflammasome improves lifespan in animal murine model of Hutchinson–Gilford ProgeriaAlvaro González‐Dominguez0Raúl Montañez1Beatriz Castejón‐Vega2Jéssica Nuñez‐Vasco3Débora Lendines‐Cordero4Chun Wang5Gabriel Mbalaviele6José M Navarro‐Pando7Elísabet Alcocer‐Gómez8Mario D Cordero9Instituto de Investigación e Innovación Biomédica de Cádiz, INiBICA, Hospital Universitario Puerta del MarInstituto de Investigación e Innovación Biomédica de Cádiz, INiBICA, Hospital Universitario Puerta del MarInstitute of Molecular, Cell and Systems Biology, University of GlasgowInstituto de Investigación e Innovación Biomédica de Cádiz, INiBICA, Hospital Universitario Puerta del MarInstituto de Investigación e Innovación Biomédica de Cádiz, INiBICA, Hospital Universitario Puerta del MarDivision of Bone and Mineral Diseases, Washington University School of MedicineDivision of Bone and Mineral Diseases, Washington University School of MedicineCátedra de Reproducción y Genética Humana del Instituto para el Estudio de la Biología de la Reproducción Humana (INEBIR), Universidad Europea del Atlántico (UNEATLANTICO)‐Fundación Universitaria Iberoamericana (FUNIBER)Departamento de Psicología Experimental, Facultad de Psicología, Universidad de SevillaInstituto de Investigación e Innovación Biomédica de Cádiz, INiBICA, Hospital Universitario Puerta del MarAbstract Inflammation is a hallmark of aging and accelerated aging syndromes such as Hutchinson–Gilford progeria syndrome (HGPS). In this study, we present evidence of increased expression of the components of the NLRP3 inflammasome pathway in HGPS skin fibroblasts, an outcome that was associated with morphological changes of the nuclei of the cells. Lymphoblasts from HGPS patients also showed increased basal levels of NLRP3 and caspase 1. Consistent with these results, the expression of caspase 1 and Nlrp3, but not of the other inflammasome receptors was higher in the heart and liver of Zmpste24−/− mice, which phenocopy the human disease. These data were further corroborated in LmnaG609G/G609G mice, another HGPS animal model. We also showed that pharmacological inhibition of the NLRP3 inflammasome by its selective inhibitor, MCC950, improved cellular phenotype, significantly extended the lifespan of progeroid animals, and reduced inflammasome‐dependent inflammation. These findings suggest that inhibition of the NLRP3 inflammasome is a potential therapeutic approach for the treatment of HGPS.https://doi.org/10.15252/emmm.202114012agingNLRP3 inflammasomeprogeria
spellingShingle Alvaro González‐Dominguez
Raúl Montañez
Beatriz Castejón‐Vega
Jéssica Nuñez‐Vasco
Débora Lendines‐Cordero
Chun Wang
Gabriel Mbalaviele
José M Navarro‐Pando
Elísabet Alcocer‐Gómez
Mario D Cordero
Inhibition of the NLRP3 inflammasome improves lifespan in animal murine model of Hutchinson–Gilford Progeria
EMBO Molecular Medicine
aging
NLRP3 inflammasome
progeria
title Inhibition of the NLRP3 inflammasome improves lifespan in animal murine model of Hutchinson–Gilford Progeria
title_full Inhibition of the NLRP3 inflammasome improves lifespan in animal murine model of Hutchinson–Gilford Progeria
title_fullStr Inhibition of the NLRP3 inflammasome improves lifespan in animal murine model of Hutchinson–Gilford Progeria
title_full_unstemmed Inhibition of the NLRP3 inflammasome improves lifespan in animal murine model of Hutchinson–Gilford Progeria
title_short Inhibition of the NLRP3 inflammasome improves lifespan in animal murine model of Hutchinson–Gilford Progeria
title_sort inhibition of the nlrp3 inflammasome improves lifespan in animal murine model of hutchinson gilford progeria
topic aging
NLRP3 inflammasome
progeria
url https://doi.org/10.15252/emmm.202114012
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