Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/20353
Full metadata record
DC FieldValueLanguage
dc.contributor.authorVassiliadis, S.en
dc.contributor.authorBalabanidou, V.en
dc.contributor.authorPapadopoulos, G. K.en
dc.contributor.authorAthanassakis, I.en
dc.date.accessioned2015-11-24T19:06:33Z-
dc.date.available2015-11-24T19:06:33Z-
dc.identifier.issn1590-8577-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/20353-
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subjectDown-Regulation/*physiologyen
dc.subjectInsulin/*biosynthesisen
dc.subjectInsulinoma/chemistry/*metabolism/pathologyen
dc.subjectInterleukin-1/*physiologyen
dc.subjectRatsen
dc.subjectReceptors, CCR3en
dc.subjectReceptors, CCR5/antagonists & inhibitors/*biosynthesis/*metabolismen
dc.subjectReceptors, Chemokine/antagonists & inhibitors/*biosynthesis/*metabolismen
dc.subjectSignal Transduction/physiologyen
dc.subjectTumor Cells, Cultureden
dc.titleLocalization and expression of CCR3 and CCR5 by interleukin-1 beta in the RIN-5AH insulin-producing model system: a protective mechanism involving down-regulation of chemokine receptorsen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/12004163-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2002-
heal.abstractCONTEXT AND OBJECTIVE: The inflammatory cytokine interleukin-1beta has been considered to be an immune effector molecule in insulin dependent diabetes mellitus. As such, we examined its role on chemokine receptors which, when expressed in the pancreas, have also been associated with the development of type I autoimmune diabetes. DESIGN AND MAIN OUTCOME MEASURES: The presence of membrane and cytoplasmic levels of CCR3 and CCR5 expression is assessed by immunofluorescence in control and interleukin-1beta-treated RIN-5AH cells. The cytoplasmic expression is also shown by confocal microscopy as assessed by the brightness of the cells whereas enzyme-linked immunosorbent assay detects secreted CCR3 and CCR5 molecules by comparing optical density values as these derive from the control and the treated cells. Cell-fractionation experiments show the exact location of the intracellular pools of the chemokine receptors by using the rab7 monoclonal antibody as a guiding molecule. RESULTS: Interleukin-1beta down-regulates constitutively expressed surface CCR3 and CCR5 levels implying receptor internalization for re-utilization or destruction, secretion or both. Cytoplasmic immunofluorescence and confocal microscopy demonstrate cellular retention of chemokine receptors by interleukin-1beta which may be released in the absence of interleukin-1beta as assessed by enzyme-linked immunosorbent assay. Finally, cell-fractionation shows the presence of both receptors in endosomes exhibiting an increasing density after interleukin-1beta treatment. CONCLUSIONS: Given the association of chemokine receptors with progression to diabetes, it appears that interleukin-1beta-induced down-regulation of CCR3 and CCR5 promotes a protective mechanism against cellular destruction. The major role of interleukin-1beta is to maintain these molecules within the endosomes. Thus, interleukin-1beta modulates the movement and the expression of constitutively expressed chemokine receptors and does not accentuate the total destructive effect suffered by the cells.en
heal.journalNameJOPen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

Files in This Item:
File Description SizeFormat 
Papadopoulos-2002-localization and expression.pdf217.29 kBAdobe PDFView/Open    Request a copy


This item is licensed under a Creative Commons License Creative Commons