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3 results on '"Jana Kubickova"'

1. Haloperidol Affects Plasticity of Differentiated NG-108 Cells Through σ1R/IP3R1 Complex

Author

Marie Nováková, Olga Krizanova, Petr Babula, Sona Hudecova, Tibor Stračina, Jana Kubickova, Lucia Csaderova, Eva Rozborilova, and Lubomira Lencesova

Subjects
0301 basic medicine, medicine.medical_specialty, Sigma-1 receptor, Endoplasmic reticulum, chemistry.chemical_element, Cell Biology, General Medicine, Calcium, Biology, 03 medical and health sciences, Cellular and Molecular Neuroscience, 030104 developmental biology, Endocrinology, chemistry, Internal medicine, Dopamine receptor D2, medicine, Unfolded protein response, Haloperidol, BD-1047, Receptor, medicine.drug
Abstract

Haloperidol is an antipsychotic agent that primarily acts as an antagonist of D2 dopamine receptors. Besides other receptor systems, it targets sigma 1 receptors (σ1Rs) and inositol 1,4,5-trisphosphate receptors (IP3Rs). Aim of this work was to investigate possible changes in IP3Rs and σ1Rs resulting from haloperidol treatment and to propose physiological consequences in differentiated NG-108 cells, i.e., effect on cellular plasticity. Haloperidol treatment resulted in up-regulation of both type 1 IP3Rs (IP3R1s) and σ1Rs at mRNA and protein levels. Haloperidol treatment did not alter expression of other types of IP3Rs. Calcium release from endoplasmic reticulum (ER) mediated by increased amount of IP3R1s elevated cytosolic calcium and generated ER stress. IP3R1s were bound to σ1Rs, and translocation of this complex from ER to nucleus occurred in the group of cells treated with haloperidol, which was followed by increased nuclear calcium levels. Haloperidol-induced changes in cytosolic, reticular, and nuclear calcium levels were similar when specific σ1 blocker -BD 1047- was used. Changes in calcium levels in nucleus, ER, and cytoplasm might be responsible for alterations in cellular plasticity, because length of neurites increased and number of neurites decreased in haloperidol-treated differentiated NG-108 cells.

Published
2017
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2. Haloperidol Affects Plasticity of Differentiated NG-108 Cells Through σ1R/IP

Author

Jana, Kubickova, Lubomira, Lencesova, Lucia, Csaderova, Tibor, Stracina, Sona, Hudecova, Petr, Babula, Eva, Rozborilova, Marie, Novakova, and Olga, Krizanova

Subjects
Neuronal Plasticity, Dose-Response Relationship, Drug, BD 1047, Cell Differentiation, NG-108 cells, Inositol 1,4,5-trisphosphate receptor, Rats, Mice, Cell Line, Tumor, Animals, Haloperidol, Inositol 1,4,5-Trisphosphate Receptors, Receptors, sigma, Sigma 1 receptor, Dopamine 2 receptor, Antipsychotic Agents, Protein Binding, Original Research
Abstract

Haloperidol is an antipsychotic agent that primarily acts as an antagonist of D2 dopamine receptors. Besides other receptor systems, it targets sigma 1 receptors (σ1Rs) and inositol 1,4,5-trisphosphate receptors (IP3Rs). Aim of this work was to investigate possible changes in IP3Rs and σ1Rs resulting from haloperidol treatment and to propose physiological consequences in differentiated NG-108 cells, i.e., effect on cellular plasticity. Haloperidol treatment resulted in up-regulation of both type 1 IP3Rs (IP3R1s) and σ1Rs at mRNA and protein levels. Haloperidol treatment did not alter expression of other types of IP3Rs. Calcium release from endoplasmic reticulum (ER) mediated by increased amount of IP3R1s elevated cytosolic calcium and generated ER stress. IP3R1s were bound to σ1Rs, and translocation of this complex from ER to nucleus occurred in the group of cells treated with haloperidol, which was followed by increased nuclear calcium levels. Haloperidol-induced changes in cytosolic, reticular, and nuclear calcium levels were similar when specific σ1 blocker -BD 1047- was used. Changes in calcium levels in nucleus, ER, and cytoplasm might be responsible for alterations in cellular plasticity, because length of neurites increased and number of neurites decreased in haloperidol-treated differentiated NG-108 cells.

Published
2016

3. Screening of Phenanthroquinolizidine Alkaloid Derivatives for Inducing Cell Death of L1210 Leukemia Cells with Negative and Positive P-glycoprotein Expression

Author

Jana Kubíčková, Katarína Elefantová, Lucia Pavlikova, Martin Cagala, Mário Šereš, Peter Šafář, Štefan Marchalín, Kamila Ďurišová, Viera Boháčová, Zdena Sulova, Boris Lakatoš, Albert Breier, and Petra Olejníková

Subjects
L1210 cells, P-glycoprotein, multidrug resistance, phenanthroquinolizidine alkaloids, apoptosis, Organic chemistry, QD241-441
Abstract

We describe the screening of a set of cryptopleurine derivatives, namely thienoquinolizidine derivatives and (epi-)benzo analogs with bioactive phenanthroquinolizidine alkaloids that induce cytotoxic effects in the mouse lymphocytic leukemia cell line L1210. We used three variants of L1210 cells: i) parental cells (S) negative for P-glycoprotein (P-gp) expression; ii) P-glycoprotein positive cells (R), obtained by selection with vincristine; iii) P-glycoprotein positive cells (T), obtained by stable transfection with a human gene encoding P-glycoprotein. We identified the most effective derivative 11 with a median lethal concentration of ≈13 μM in all three L1210 cell variants. The analysis of the apoptosis/necrosis induced by derivative 11 revealed that cell death was the result of apoptosis with late apoptosis characteristics. Derivative 11 did not induce a strong alteration in the proportion of cells in the G1, S or G2/M phase of the cell cycle, but a strong increase in the number of S, R and T cells in the subG1 phase was detected. These findings indicated that we identified the most effective inducer of cell death, derivative 11, and this derivative effectively induced cell death in S, R and T cells at similar inhibitory concentrations independent of P-gp expression.

Published
2019
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