TY  - JOUR
AU  - Srdić-Rajić, Tatjana
AU  - Nikolić, Katarina
AU  - Cavić, Milena
AU  - Đokić, Ivana
AU  - Gemović, Branislava
AU  - Perović, Vladimir
AU  - Veljković, Nevena
PY  - 2016
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/2578
AB  - Imidazoline 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.
PB  - Elsevier Science BV, Amsterdam
T2  - European Journal of Pharmaceutical Sciences
T1  - Rilmenidine suppresses proliferation and promotes apoptosis via the mitochondrial pathway in human leukemic K562 cells
VL  - 81
SP  - 172
EP  - 180
DO  - 10.1016/j.ejps.2015.10.017
ER  - 

@article{
author = "Srdić-Rajić, Tatjana and Nikolić, Katarina and Cavić, Milena and Đokić, Ivana and Gemović, Branislava and Perović, Vladimir and Veljković, Nevena",
year = "2016",
abstract = "Imidazoline 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.",
publisher = "Elsevier Science BV, Amsterdam",
journal = "European Journal of Pharmaceutical Sciences",
title = "Rilmenidine suppresses proliferation and promotes apoptosis via the mitochondrial pathway in human leukemic K562 cells",
volume = "81",
pages = "172-180",
doi = "10.1016/j.ejps.2015.10.017"
}

Srdić-Rajić, T., Nikolić, K., Cavić, M., Đokić, I., Gemović, B., Perović, V.,& Veljković, N.. (2016). Rilmenidine suppresses proliferation and promotes apoptosis via the mitochondrial pathway in human leukemic K562 cells. in European Journal of Pharmaceutical Sciences
Elsevier Science BV, Amsterdam., 81, 172-180.
https://doi.org/10.1016/j.ejps.2015.10.017

Srdić-Rajić T, Nikolić K, Cavić M, Đokić I, Gemović B, Perović V, Veljković N. Rilmenidine suppresses proliferation and promotes apoptosis via the mitochondrial pathway in human leukemic K562 cells. in European Journal of Pharmaceutical Sciences. 2016;81:172-180.
doi:10.1016/j.ejps.2015.10.017 .

Srdić-Rajić, Tatjana, Nikolić, Katarina, Cavić, Milena, Đokić, Ivana, Gemović, Branislava, Perović, Vladimir, Veljković, Nevena, "Rilmenidine suppresses proliferation and promotes apoptosis via the mitochondrial pathway in human leukemic K562 cells" in European Journal of Pharmaceutical Sciences, 81 (2016):172-180,
https://doi.org/10.1016/j.ejps.2015.10.017 . .