Sex-Specific Effects of the Nlrp3 Inflammasome on Atherogenesis in LDL Receptor-Deficient Mice

In the Ldlr(-/-) mouse model of atherosclerosis, female Nlrp3(-/-) bone marrow chimera and Nlrp3(-/-) mice developed significantly smaller lesions in the aortic sinus and decreased lipid content in aorta en face, but a similar protection was not observed in males. Ovariectomized female mice lost pro...

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Detalles Bibliográficos
Autores principales: Chen, Shuang, Markman, Janet L., Shimada, Kenichi, Crother, Timothy R., Lane, Malcolm, Abolhesn, Amanda, Shah, Prediman K., Arditi, Moshe
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2020
Materias:
PRECLINICAL RESEARCH
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7315187/
https://www.ncbi.nlm.nih.gov/pubmed/32613145
http://dx.doi.org/10.1016/j.jacbts.2020.03.016
Descripción
Sumario:In the Ldlr(-/-) mouse model of atherosclerosis, female Nlrp3(-/-) bone marrow chimera and Nlrp3(-/-) mice developed significantly smaller lesions in the aortic sinus and decreased lipid content in aorta en face, but a similar protection was not observed in males. Ovariectomized female mice lost protection from atherosclerosis in the setting of NLRP3 deficiency, whereas atherosclerosis showed a greater dependency on NLRP3 in castrated males. Thus, castration increased the dependency of atherosclerosis on the NLRP3 inflammasome, suggesting that testosterone may block inflammation in atherogenesis. Conversely, ovariectomy reduced the dependency on NLRP3 inflammasome components for atherogenesis, suggesting that estrogen may promote inflammasome-mediated atherosclerosis.

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