Cholesterol depletion induces PKA-mediated basolateral-to-apical transcytosis of the scavenger receptor class B type I in MDCK cells

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dc.contributor.authorBurgos, PV
dc.contributor.authorKlattenhoff, C
dc.contributor.authorde la Fuente, E
dc.contributor.authorRigotti, A
dc.contributor.authorGonzalez, A
dc.date.accessioned2024-01-10T13:11:42Z
dc.date.available2024-01-10T13:11:42Z
dc.date.issued2004
dc.description.abstractCholesterol-based membrane microdomains, or lipid rafts, are believed to play important, yet poorly defined, roles in protein trafficking and signal transduction. In polarized epithelial cells, the current view is that rafts are involved in apical but not in basolateral protein transport from the trans-Golgi network (TGN). We report here that cholesterol is required in a post-TGN mechanism of basolateral regionalization. Permanently transfected Madin-Darby canine kidney cells segregated the caveolae/raft-associated high-density lipoprotein scavenger receptor class B type I (SR-BI) predominantly to the basolateral domain where it was constitutively internalized and recycled basolaterally. Acute cholesterol depletion did not significantly alter SR-BI internalization, implying a cholesterol depletion-insensitive endocytic process but instead induced its transcytosis through a protein kinase A (PKA)- and microtubule-dependent mechanism. Forskolin also elicited SR-BI transcytosis. The basolateral distribution of endogenous epidermal growth factor receptor remained unaffected. Strikingly, cholesterol depletion induced PKA activity without increasing the cAMP levels. Thus, our results are consistent with a scenario in which cholesterol-based rafts promote internalization and basolateral recycling of internalized SR-BI whereas a PKA pool sensitive to cholesterol depletion mediates SR-BI transcytosis. Regulated transcytosis of SR-BI may provide an additional mechanism to control cholesterol homeostasis. These results disclose relationships between cholesterol-based rafts and PKA activity operating in a post-TGN mechanism of regulated apical-to-basolateral cell surface protein distribution.
dc.fechaingreso.objetodigital2024-05-06
dc.format.extent6 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1073/pnas.0400295101
dc.identifier.issn0027-8424
dc.identifier.pubmedidMEDLINE:15007173
dc.identifier.urihttps://doi.org/10.1073/pnas.0400295101
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/78084
dc.identifier.wosidWOS:000220314500025
dc.information.autorucMedicina;Rigotti A;S/I;68489
dc.issue.numero11
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final3850
dc.pagina.inicio3845
dc.publisherNATL ACAD SCIENCES
dc.revistaPROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
dc.rightsacceso restringido
dc.subjectDENSITY-LIPOPROTEIN-RECEPTOR
dc.subjectGROWTH-FACTOR RECEPTOR
dc.subjectPROTEIN-TYROSINE PHOSPHORYLATION
dc.subjectPLASMA-MEMBRANE PROTEINS
dc.subjectGPI-ANCHORED PROTEINS
dc.subjectCANINE KIDNEY-CELLS
dc.subjectSR-BI
dc.subjectLIPID RAFTS
dc.subjectSIGNAL-TRANSDUCTION
dc.subjectEPITHELIAL-CELLS
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleCholesterol depletion induces PKA-mediated basolateral-to-apical transcytosis of the scavenger receptor class B type I in MDCK cells
dc.typeartículo
dc.volumen101
sipa.codpersvinculados68489
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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