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Título: | SFRP1 modulates astrocyte-to-microglia crosstalk in acute and chronic neuroinflammation |
Autor: | Rueda-Carrasco, Javier; Martín-Bermejo, María Jesús CSIC; Pereyra, Guadalupe; Mateo, María Inés; Borroto, Aldo; Brosseron, Frederic; Kummer, Markus P.; Schwartz, Stephanie; López-Atalaya, José P. CSIC ORCID; Alarcón, Balbino CSIC ORCID; Esteve, Pilar CSIC ORCID ; Heneka, Michael T.; Bovolenta, Paola CSIC ORCID | Palabras clave: | Activated microglia Alzheimer’s disease HIF pathway Multiple sclerosis Reactive astrocytes |
Fecha de publicación: | 2021 | Editor: | EMBO Press | Citación: | EMBO Reports 22: e51696 (2021) | Resumen: | Neuroinflammation is a common feature of many neurodegenerative diseases. It fosters a dysfunctional neuron–microglia–astrocyte crosstalk that, in turn, maintains microglial cells in a perniciously reactive state that often enhances neuronal damage. The molecular components that mediate this critical communication are not fully explored. Here, we show that secreted frizzled-related protein 1 (SFRP1), a multifunctional regulator of cell-to-cell communication, is part of the cellular crosstalk underlying neuroinflammation. In mouse models of acute and chronic neuroinflammation, SFRP1, largely astrocyte-derived, promotes and sustains microglial activation, and thus a chronic inflammatory state. SFRP1 promotes the upregulation of components of the hypoxia-induced factor-dependent inflammatory pathway and, to a lower extent, of those downstream of the nuclear factor-kappa B. We thus propose that SFRP1 acts as an astrocyte-to-microglia amplifier of neuroinflammation, representing a potential valuable therapeutic target for counteracting the harmful effect of chronic inflammation in several neurodegenerative diseases. | Versión del editor: | https://doi.org/10.15252/embr.202051696 | URI: | http://hdl.handle.net/10261/267644 | DOI: | 10.15252/embr.202051696 | E-ISSN: | 1469-3178 |
Aparece en las colecciones: | (IN) Artículos (CBM) Artículos |
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sfrp1.pdf | 4,22 MB | Adobe PDF | Visualizar/Abrir |
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