2026-07-21T21:47:35Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/96322024-10-31T11:45:07Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605col_20.500.12105_19607
Repisalud
author
Casanova-Acebes, Maria
author
Menendez-Gutierrez, Maria Piedad
author
Porcuna, Jesus
author
Alvarez-Errico, Damiana
author
Lavin, Yonit
author
Garcia, Ana
author
Kobayashi, Soma
author
Le Berichel, Jessica
author
Nunez, Vanessa
author
Were, Felipe
author
Jimenez-Carretero, Daniel
author
Sanchez-Cabo, Fatima
author
Merad, Miriam
author
Ricote, Mercedes
funder
Ministerio de Ciencia, Innovación y Universidades (España)
funder
Fundación La Marató TV3
funder
Comunidad de Madrid (España)
funder
Fundación ProCNIC
2020-04-20T13:46:47Z
2020-04-20T13:46:47Z
2020-04-03
Nat Commun. 2020; 11(1):1655
10.1038/s41467-020-15371-0
2041-1723
2041-1723
Nature communications
32246014
http://hdl.handle.net/20.500.12105/9632
Tissue-resident macrophages (TRMs) populate all tissues and play key roles in homeostasis, immunity and repair. TRMs express a molecular program that is mostly shaped by tissue cues. However, TRM identity and the mechanisms that maintain TRMs in tissues remain poorly understood. We recently found that serous-cavity TRMs (LPMs) are highly enriched in RXR transcripts and RXR-response elements. Here, we show that RXRs control mouse serous-macrophage identity by regulating chromatin accessibility and the transcriptional regulation of canonical macrophage genes. RXR deficiency impairs neonatal expansion of the LPM pool and reduces the survival of adult LPMs through excess lipid accumulation. We also find that peritoneal LPMs infiltrate early ovarian tumours and that RXR deletion diminishes LPM accumulation in tumours and strongly reduces ovarian tumour progression in mice. Our study reveals that RXR signalling controls the maintenance of the serous macrophage pool and that targeting peritoneal LPMs may improve ovarian cancer outcomes.
eng
RXRs control serous macrophage neonatal expansion and identity and contribute to ovarian cancer progression
journal article
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