17 beta-estradiol modulates mitochondrial Ca2+ flux in rat caudate nucleus and brain stem
Nema prikaza
Autori
Petrović, SnježanaMilošević, Maja
Drakulić, Dunja R.
Grković, Ivana
Stanojlović, Miloš R.
Mitrović, Nataša Lj.
Horvat, Anica
Članak u časopisu
Metapodaci
Prikaz svih podataka o dokumentuApstrakt
The aim of this study was to examine the rapid non-genomic effect of 17 beta-estradiol (E2) on Ca2+ transport in mitochondria isolated from the nerve terminals (synaptosomes) of caudate nuclei (NC) and brain stems (BS) of ovariectomised female rats. In physiological conditions no effect of E2 on Ca2+ influx into synaptosomal mitochondria through ruthenium red (RR)-sensitive uniporter was observed. However, in the presence of uncoupling agent carbonyl cyanide4-(trifluoromethoxy)phenylhydrazone (FCCP) (1 mu mol/l), pre-treatment with 0.5 nmol/l E2 protected mitochondrial membrane potential and consequently increased Ca2+ influx (2.3-fold in NC and 3.1-fold in BS). At the same time, 0.5 nmol/l E2 by increasing the affinity of mitochondrial Na+/Ca2+ exchanger for Na+ inhibited mitochondrial Ca2+ efflux in NC and BS by about 40%. Also, the specific binding of physiological E2 concentrations (0.1-10 nmol/l) to isolated synaptosomal mitochondria was detected. Using membrane impermeable E2 bou...nd to bovine serum albumin and selective inhibitor of mitochondrial Na+/Ca2+ exchanger, we obtained that E2s action on mitochondrial Ca2+ efflux at least partially is due to the direct effects on the mitochondrial membrane and/or Na+/Ca2+ exchanger located in inner mitochondrial membrane. Our results implicate E2 as a modulator of Ca2+ concentration in mitochondrial matrix, and ultimately in the cytosol. Given the vital role of Ca2+ in regulation of total nerve cells activity, especially energy metabolism, neurotransmission and directing the cells toward survival or cell death, the effects on mitochondrial Ca2+ transport could be one of the important modes of E2 neuromodulatory action independent of the genome. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.
Ključne reči:
synaptosomal mitochondria / Ca2+ transport / estradiol / rat brain / caudate nucleus / brain stemIzvor:
Neuroscience, 2012, 220, 32-40Finansiranje / projekti:
- Molekularni mehanizmi patofizioloških promena u ćelijama centralnog nervnog sistema i perifernog tkiva kod sisara (RS-MESTD-Basic Research (BR or ON)-173044)
DOI: 10.1016/j.neuroscience.2012.06.040
ISSN: 0306-4522
PubMed: 22735576
WoS: 000307802100005
Scopus: 2-s2.0-84864780476
Kolekcije
Institucija/grupa
VinčaTY - JOUR AU - Petrović, Snježana AU - Milošević, Maja AU - Drakulić, Dunja R. AU - Grković, Ivana AU - Stanojlović, Miloš R. AU - Mitrović, Nataša Lj. AU - Horvat, Anica PY - 2012 UR - https://vinar.vin.bg.ac.rs/handle/123456789/5012 AB - The aim of this study was to examine the rapid non-genomic effect of 17 beta-estradiol (E2) on Ca2+ transport in mitochondria isolated from the nerve terminals (synaptosomes) of caudate nuclei (NC) and brain stems (BS) of ovariectomised female rats. In physiological conditions no effect of E2 on Ca2+ influx into synaptosomal mitochondria through ruthenium red (RR)-sensitive uniporter was observed. However, in the presence of uncoupling agent carbonyl cyanide4-(trifluoromethoxy)phenylhydrazone (FCCP) (1 mu mol/l), pre-treatment with 0.5 nmol/l E2 protected mitochondrial membrane potential and consequently increased Ca2+ influx (2.3-fold in NC and 3.1-fold in BS). At the same time, 0.5 nmol/l E2 by increasing the affinity of mitochondrial Na+/Ca2+ exchanger for Na+ inhibited mitochondrial Ca2+ efflux in NC and BS by about 40%. Also, the specific binding of physiological E2 concentrations (0.1-10 nmol/l) to isolated synaptosomal mitochondria was detected. Using membrane impermeable E2 bound to bovine serum albumin and selective inhibitor of mitochondrial Na+/Ca2+ exchanger, we obtained that E2s action on mitochondrial Ca2+ efflux at least partially is due to the direct effects on the mitochondrial membrane and/or Na+/Ca2+ exchanger located in inner mitochondrial membrane. Our results implicate E2 as a modulator of Ca2+ concentration in mitochondrial matrix, and ultimately in the cytosol. Given the vital role of Ca2+ in regulation of total nerve cells activity, especially energy metabolism, neurotransmission and directing the cells toward survival or cell death, the effects on mitochondrial Ca2+ transport could be one of the important modes of E2 neuromodulatory action independent of the genome. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved. T2 - Neuroscience T1 - 17 beta-estradiol modulates mitochondrial Ca2+ flux in rat caudate nucleus and brain stem VL - 220 SP - 32 EP - 40 DO - 10.1016/j.neuroscience.2012.06.040 ER -
@article{ author = "Petrović, Snježana and Milošević, Maja and Drakulić, Dunja R. and Grković, Ivana and Stanojlović, Miloš R. and Mitrović, Nataša Lj. and Horvat, Anica", year = "2012", abstract = "The aim of this study was to examine the rapid non-genomic effect of 17 beta-estradiol (E2) on Ca2+ transport in mitochondria isolated from the nerve terminals (synaptosomes) of caudate nuclei (NC) and brain stems (BS) of ovariectomised female rats. In physiological conditions no effect of E2 on Ca2+ influx into synaptosomal mitochondria through ruthenium red (RR)-sensitive uniporter was observed. However, in the presence of uncoupling agent carbonyl cyanide4-(trifluoromethoxy)phenylhydrazone (FCCP) (1 mu mol/l), pre-treatment with 0.5 nmol/l E2 protected mitochondrial membrane potential and consequently increased Ca2+ influx (2.3-fold in NC and 3.1-fold in BS). At the same time, 0.5 nmol/l E2 by increasing the affinity of mitochondrial Na+/Ca2+ exchanger for Na+ inhibited mitochondrial Ca2+ efflux in NC and BS by about 40%. Also, the specific binding of physiological E2 concentrations (0.1-10 nmol/l) to isolated synaptosomal mitochondria was detected. Using membrane impermeable E2 bound to bovine serum albumin and selective inhibitor of mitochondrial Na+/Ca2+ exchanger, we obtained that E2s action on mitochondrial Ca2+ efflux at least partially is due to the direct effects on the mitochondrial membrane and/or Na+/Ca2+ exchanger located in inner mitochondrial membrane. Our results implicate E2 as a modulator of Ca2+ concentration in mitochondrial matrix, and ultimately in the cytosol. Given the vital role of Ca2+ in regulation of total nerve cells activity, especially energy metabolism, neurotransmission and directing the cells toward survival or cell death, the effects on mitochondrial Ca2+ transport could be one of the important modes of E2 neuromodulatory action independent of the genome. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.", journal = "Neuroscience", title = "17 beta-estradiol modulates mitochondrial Ca2+ flux in rat caudate nucleus and brain stem", volume = "220", pages = "32-40", doi = "10.1016/j.neuroscience.2012.06.040" }
Petrović, S., Milošević, M., Drakulić, D. R., Grković, I., Stanojlović, M. R., Mitrović, N. Lj.,& Horvat, A.. (2012). 17 beta-estradiol modulates mitochondrial Ca2+ flux in rat caudate nucleus and brain stem. in Neuroscience, 220, 32-40. https://doi.org/10.1016/j.neuroscience.2012.06.040
Petrović S, Milošević M, Drakulić DR, Grković I, Stanojlović MR, Mitrović NL, Horvat A. 17 beta-estradiol modulates mitochondrial Ca2+ flux in rat caudate nucleus and brain stem. in Neuroscience. 2012;220:32-40. doi:10.1016/j.neuroscience.2012.06.040 .
Petrović, Snježana, Milošević, Maja, Drakulić, Dunja R., Grković, Ivana, Stanojlović, Miloš R., Mitrović, Nataša Lj., Horvat, Anica, "17 beta-estradiol modulates mitochondrial Ca2+ flux in rat caudate nucleus and brain stem" in Neuroscience, 220 (2012):32-40, https://doi.org/10.1016/j.neuroscience.2012.06.040 . .