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dc.creatorSrdić-Rajić, Tatjana
dc.creatorNikolic, Katarina
dc.creatorCavic, Milena
dc.creatorĐokić, Ivana
dc.creatorGemović, Branislava S.
dc.creatorPerović, Vladimir R.
dc.creatorVeljković, Nevena V.
dc.date.accessioned2018-03-01T16:37:20Z
dc.date.available2018-03-01T16:37:20Z
dc.date.issued2016
dc.identifier.issn0928-0987 (print)
dc.identifier.issn1879-0720 (electronic)
dc.identifier.urihttp://vinar.vin.bg.ac.rs/handle/123456789/884
dc.description.abstractImidazoline I1 receptor signaling is associated with pathways that regulate cell viability leading to varied cell-type specific phenotypes. We demonstrated that the antihypertensive drug rilmenidine, a selective imidazoline I1 receptor agonist, modulates proliferation and stimulates the proapoptotic protein Bax thus inducing the perturbation of the mitochondrial pathway and apoptosis in human leukemic K562 cells. Rilmenidine acts through a mechanism which involves deactivation of Ras/MAP kinases ERK, p38 and JNK. Moreover, rilmenidine renders K562 cells, which are particularly resistant to chemotherapeutic agents, susceptible to the DNA damaging drug doxorubicin. The rilmenidine co-treatment with doxorubicin reverses G2/M arrest and triggers apoptotic response to DNA damage. Our data offer new insights into the pathways associated with imidazoline I1 receptor activation in K562 cells suggesting rilmenidine as a valuable tool to deepen our understanding of imidazoline I1 receptor signaling in hematologic malignancies and to search for medicinally active agents. (C) 2015 Elsevier B.V. All rights reserved.en
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173001/RS//
dc.relationinfo:eu-repo/grantAgreement/MESTD/Integrated and Interdisciplinary Research (IIR or III)/41026/RS//
dc.rightsrestrictedAccessen
dc.sourceEuropean Journal of Pharmaceutical Sciencesen
dc.subjectRilmenidineen
dc.subjectImidazoline I1 receptor signalingen
dc.subjectApoptosisen
dc.subjectProliferationen
dc.subjectK562en
dc.subjectDNA damageen
dc.titleRilmenidine suppresses proliferation and promotes apoptosis via the mitochondrial pathway in human leukemic K562 cellsen
dc.typearticleen
dcterms.abstractНиколиц, Катарина; Срдиц-Рајиц, Татјана; Дјокиц, Ивана; Гемовић Бранислава; Цавиц, Милена; Перовић Владимир; Вељковић Невена В.;
dc.citation.volume81
dc.citation.spage172
dc.citation.epage180
dc.identifier.wos000367787700021
dc.identifier.doi10.1016/j.ejps.2015.10.017
dc.citation.rankM21
dc.identifier.pmid26598394
dc.identifier.scopus2-s2.0-84946239745


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