2026-06-30T04:57:34Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/65152024-09-27T08:45:14Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Rey-Barroso, Javier
author
Alvarez-Barrientos, Alberto
author
Rico-Leo, Eva
author
Contador-Troca, Maria
author
Carvajal-Gonzalez, Jose M.
author
Echarri, Asier
author
del Pozo, Miguel Angel
author
Fernandez-Salguero, Pedro M.
funder
Ministerio de Ciencia e Innovación (España)
funder
Government of Extremadura (España)
funder
Red Temática de Investigación Cooperativa en Cáncer (RTICC) (España)
funder
Instituto de Salud Carlos III
funder
Ministerio de Sanidad, Servicios Sociales e Igualdad (España)
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
2018-10-25T08:19:45Z
2018-10-25T08:19:45Z
2014
Cell Commun Signal. 2014; 12(1):57
10.1186/s12964-014-0057-7
1478-811X
Cell Communication and Signaling
25238970
http://hdl.handle.net/20.500.12105/6515
Background: Adhesion and migration are relevant physiological functions that must be regulated by the cell under both normal and pathological conditions. The dioxin receptor (AhR) has emerged as a transcription factor regulating both processes in mesenchymal, epithelial and endothelial cells. Indirect results suggest that AhR could cooperate not only with additional transcription factors but also with membrane-associated proteins to drive such processes. Results: In this study, we have used immortalized and primary dermal fibroblasts from wild type (AhR+/+) and AhR-null (AhR-/-) mice to show that AhR modulates membrane distribution and mobilization of caveolin-1 (Cav-1) during directional cell migration. AhR co-immunoprecipitated with Cav-1 and a fraction of both proteins co-localized to detergent-resistant membrane microdomains (DRM). Consistent with a role of AhR in the process, AhR-/-cells had a significant reduction in Cav-1 in DRMs. Moreover, high cell density reduced AhR nuclear levels and moved Cav-1 from DRMs to the soluble membrane in AhR+/+ but not in AhR-/-cells. Tyrosine-14 phosphorylation had a complex role in the mechanism since its upregulation reduced Cav-1 in DRMs in both AhR+/+ and AhR-/-cells, despite the lower basal levels of Y-14-Cav-1 in the null cells. Fluorescence recovery after photobleaching revealed that AhR knock-down blocked Cav-1 transport to the plasma membrane, a deficit possibly influencing its depleted levels in DRMs. Membrane distribution of Cav-1 in AhR-null fibroblasts correlated with higher levels of cholesterol and with disrupted membrane microdomains, whereas addition of exogenous cholesterol changed the Cav-1 distribution of AhR+/+ cells to the null phenotype. Consistently, higher cholesterol levels enhanced caveolae-dependent endocytosis in AhR-null cells. Conclusions: These results suggest that AhR modulates Cav-1 distribution in migrating cells through the control of cholesterol-enriched membrane microdomains. Our study also supports the likely possibility of membrane-related, transcription factor independent, functions of AhR.
eng
Dioxin receptor
Caveolin-1
Membrane microdomains
Endocytosis
Cholesterol
ARYL-HYDROCARBON RECEPTOR
ENDOTHELIAL-CELLS
IN-VIVO
NUCLEAR TRANSLOCATION
DEPENDENT MECHANISM
LIPID BODIES
TGF-BETA
EXPRESSION
POLARIZATION
FIBROBLASTS
The Dioxin receptor modulates Caveolin-1 mobilization during directional migration: role of cholesterol
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