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Title: Crosstalk between LXR and caveolin-1 signaling supports cholesterol efflux and anti-inflammatory pathways in macrophages
Authors: Ramírez, Cristina M.
Torrecilla, M.
Pardo, Virginia
Fernández, Mario
Pérez, Ana
Tabraue Tarbay, Carlos 
De La Rosa Medina, Juan Vladimir 
Martín Rodríguez, Patricia 
Díaz Sarmiento, María Mercedes 
Celorio, Marta
Traves, Paqui G.
Camps, Marta
Boscá, Lisardo
Núñez, Uxue
Castrillo Viguera, Antonio Jesús 
UNESCO Clasification: 320502 Endocrinología
2403 Bioquímica
Keywords: Caveolin-1
Cholesterol Efflux
Gene Expression
Lxr, et al
Issue Date: 2021
Journal: Frontiers in Endocrinology 
Abstract: Macrophages are immune cells that play crucial roles in host defense against pathogens by triggering their exceptional phagocytic and inflammatory functions. Macrophages that reside in healthy tissues also accomplish important tasks to preserve organ homeostasis, including lipid uptake/efflux or apoptotic-cell clearance. Both homeostatic and inflammatory functions of macrophages require the precise stability of lipid-rich microdomains located at the cell membrane for the initiation of downstream signaling cascades. Caveolin-1 (Cav-1) is the main protein responsible for the biogenesis of caveolae and plays an important role in vascular inflammation and atherosclerosis. The Liver X receptors (LXRs) are key transcription factors for cholesterol efflux and inflammatory gene responses in macrophages. Although the role of Cav-1 in cellular cholesterol homeostasis and vascular inflammation has been reported, the connection between LXR transcriptional activity and Cav-1 expression and function in macrophages has not been investigated. Here, using gain and loss of function approaches, we demonstrate that LXR-dependent transcriptional pathways modulate Cav-1 expression and compartmentation within the membrane during macrophage activation. As a result, Cav-1 participates in LXR-dependent cholesterol efflux and the control of inflammatory responses. Together, our data show modulation of the LXR-Cav-1 axis could be exploited to control exacerbated inflammation and cholesterol overload in the macrophage during the pathogenesis of lipid and immune disorders, such as atherosclerosis
ISSN: 1664-2392
DOI: 10.3389/fendo.2021.635923
Source: Frontiers in Endocrinology [EISSN 1664-2392],v. 12, (Mayo 2021)
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