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Potential role of proteasome on c-jun related signaling in hypercholesterolemia induced atherosclerosis

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dc.contributor.authorSÖZEN, AHMET ERDİ
dc.contributor.authorsSozen, Erdi; Karademir, Betul; Yazgan, Burak; Bozaykut, Perinur; Ozer, Nesrin Kartal
dc.date.accessioned2022-03-14T10:19:19Z
dc.date.available2022-03-14T10:19:19Z
dc.date.issued2014
dc.description.abstractAtherosclerosis and its complications are major causes of death all over the world. One of the major risks of atherosclerosis is hypercholesterolemia. During atherosclerosis, oxidized low density lipoprotein (oxLDL) regulates CD36-mediated activation of c-jun amino terminal kinase-1 (JNK1) and modulates matrix metalloproteinase (MMP) induction which stimulates inflammation with an invasion of monocytes. Additionally, inhibition of proteasome leads to an accumulation of c-jun and phosphorylated c-jun and activation of activator protein-1 (AP-1) related increase of MMP expression. We have previously reported a significant increase in cluster of differentiation 36 (CD36) mRNA levels in hypercholesterolemic rabbits and shown that vitamin E treatment prevented the cholesterol induced increase in CD36 mRNA expression. In the present study, our aim is to identify the signaling molecules/transcription factors involved in the progression of atherosclerosis following CD36 activation in an in vivo model of hypercholesterolemic (induced by 2% cholesterol containing diet) rabbits. In this direction, proteasomal activities by fluorometry and c-jun, phospo c-jun, JNK1, MMP-9 expressions by quantitative RT-PCR and immunoblotting were tested in aortic tissues. The effects of vitamin E on these changes were also investigated in this model. As a result, c-jun was phosphorylated following decreased proteasomal degradation in hypercholesterolemic group. MMP-9 expression was also increased in cholesterol group rabbits contributing to the development of atherosclerosis. In addition, vitamin E showed its effect by decreasing MMP-9 levels and phosphorylation of c-jun. (C) 2014 The Authors. Published by Elsevier B.V.
dc.identifier.doi10.1016/j.redox.2014.02.007
dc.identifier.issn2213-2317
dc.identifier.pubmed25009774
dc.identifier.urihttps://hdl.handle.net/11424/244348
dc.identifier.wosWOS:000350769600086
dc.language.isoeng
dc.publisherELSEVIER SCIENCE BV
dc.relation.ispartofREDOX BIOLOGY
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAtherosclerosis
dc.subjectHypercholesterolemia
dc.subjectProteasome
dc.subjectJNK1
dc.subjectAP-1
dc.subjectVitamin E
dc.subjectSMOOTH-MUSCLE-CELLS
dc.subjectSCAVENGER RECEPTOR EXPRESSION
dc.subjectACTIVATED PROTEIN-KINASES
dc.subjectVITAMIN-E
dc.subjectOXIDIZED LDL
dc.subjectOXIDATIVE STRESS
dc.subjectTRANSCRIPTION FACTOR
dc.subjectMAP KINASES
dc.subjectIN-VITRO
dc.subjectRABBITS
dc.titlePotential role of proteasome on c-jun related signaling in hypercholesterolemia induced atherosclerosis
dc.typearticle
dspace.entity.typePublication
local.avesis.id20a05ebc-1669-4aa0-9118-900c7b80d78a
local.import.packageSS16
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages7
oaire.citation.endPage738
oaire.citation.startPage732
oaire.citation.titleREDOX BIOLOGY
oaire.citation.volume2
relation.isAuthorOfPublication47991a21-cce9-4b87-b091-bede64f8b4e0
relation.isAuthorOfPublication.latestForDiscovery47991a21-cce9-4b87-b091-bede64f8b4e0

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