Estradiol receptors mediate estradiol-induced inhibition of mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem
Само за регистроване кориснике
2015
Аутори
Petrović, SnježanaMilošević, Maja
Ristic-Medic, Danijela
Velickovic, Natasa
Drakulić, Dunja R.
Grković, Ivana
Horvat, Anica
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт
Our earlier studies found that in vitro estradiol modulates mitochondrial Ca2+ transport in discrete brain regions. The present study examined the role of estradiol receptors (ERs) in estradiol-induced inhibition of Ca2+ efflux from synaptosomal mitochondria isolated from rat caudate nuclei and brain stems. Radioactively labeled CaCl2 (0.6-0.75 mu Ci (CaCl2)-Ca-45) was used for Ca2+ transport monitoring. The results revealed that in the presence of ER antagonist 7 alpha, 17 beta-[9[(4,4,5,5,5-pentafluoropentyl) sulfinyl] nonyl] estra-1,3,5( 10)-triene-3,17-diol (ICI 182,780) (1 mu mol/L), the inhibitory effect of estradiol on mitochondrial Ca2+ efflux was more than 60% decreased, suggesting the involvement of ER in this mode of estradiol neuromodulatory action. When particular contributions of ER alpha and ER beta were tested, it was found that ER beta agonist 2,3-bis(4-hydroxy phenyl)-propionitrile (10 nmol/L) inhibited Ca2+ efflux more than 20%, while the inhibition with ER alpha ago...nist 4,4, 4-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (10 nmol/L) was about 10%, both compared to the control. Both agonists demonstrated attenuation of Ca2+ efflux decrease in the presence of mitochondrial Na+/Ca2+ exchanger antagonist 7-chloro-5-(2-chlorophenyl)-1,5-dihyhdro-4,1-benzothiazepin-2(3H)-one (10 mu mol/L), showing interference with the inhibitory action of that agent. Our results strongly indicate ERs as the mediators of estradiol-induced mitochondrial Ca2+ efflux inhibition in rat caudate nucleus and brain stem synaptosomes.
Кључне речи:
Ca2+ efflux / estradiol receptors / synaptosomal mitochondria / caudate nucleus / brain stemИзвор:
Turkish Journal of Biology, 2015, 39, 2, 328-334Финансирање / пројекти:
- Молекуларни механизми патофизиолошких промена у ћелијама централног нервног система и периферног ткива код сисара (RS-MESTD-Basic Research (BR or ON)-173044)
- Биолошки механизми, нутритивни унос и статус полинезасићених масних киселина и фолата: Унапређење исхране у Србији (RS-MESTD-Integrated and Interdisciplinary Research (IIR or III)-41030)
DOI: 10.3906/biy-1408-62
ISSN: 1300-0152; 1303-6092
WoS: 000352483900019
Scopus: 2-s2.0-84928982187
Колекције
Институција/група
VinčaTY - JOUR AU - Petrović, Snježana AU - Milošević, Maja AU - Ristic-Medic, Danijela AU - Velickovic, Natasa AU - Drakulić, Dunja R. AU - Grković, Ivana AU - Horvat, Anica PY - 2015 UR - https://vinar.vin.bg.ac.rs/handle/123456789/495 AB - Our earlier studies found that in vitro estradiol modulates mitochondrial Ca2+ transport in discrete brain regions. The present study examined the role of estradiol receptors (ERs) in estradiol-induced inhibition of Ca2+ efflux from synaptosomal mitochondria isolated from rat caudate nuclei and brain stems. Radioactively labeled CaCl2 (0.6-0.75 mu Ci (CaCl2)-Ca-45) was used for Ca2+ transport monitoring. The results revealed that in the presence of ER antagonist 7 alpha, 17 beta-[9[(4,4,5,5,5-pentafluoropentyl) sulfinyl] nonyl] estra-1,3,5( 10)-triene-3,17-diol (ICI 182,780) (1 mu mol/L), the inhibitory effect of estradiol on mitochondrial Ca2+ efflux was more than 60% decreased, suggesting the involvement of ER in this mode of estradiol neuromodulatory action. When particular contributions of ER alpha and ER beta were tested, it was found that ER beta agonist 2,3-bis(4-hydroxy phenyl)-propionitrile (10 nmol/L) inhibited Ca2+ efflux more than 20%, while the inhibition with ER alpha agonist 4,4, 4-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (10 nmol/L) was about 10%, both compared to the control. Both agonists demonstrated attenuation of Ca2+ efflux decrease in the presence of mitochondrial Na+/Ca2+ exchanger antagonist 7-chloro-5-(2-chlorophenyl)-1,5-dihyhdro-4,1-benzothiazepin-2(3H)-one (10 mu mol/L), showing interference with the inhibitory action of that agent. Our results strongly indicate ERs as the mediators of estradiol-induced mitochondrial Ca2+ efflux inhibition in rat caudate nucleus and brain stem synaptosomes. T2 - Turkish Journal of Biology T1 - Estradiol receptors mediate estradiol-induced inhibition of mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem VL - 39 IS - 2 SP - 328 EP - 334 DO - 10.3906/biy-1408-62 ER -
@article{ author = "Petrović, Snježana and Milošević, Maja and Ristic-Medic, Danijela and Velickovic, Natasa and Drakulić, Dunja R. and Grković, Ivana and Horvat, Anica", year = "2015", abstract = "Our earlier studies found that in vitro estradiol modulates mitochondrial Ca2+ transport in discrete brain regions. The present study examined the role of estradiol receptors (ERs) in estradiol-induced inhibition of Ca2+ efflux from synaptosomal mitochondria isolated from rat caudate nuclei and brain stems. Radioactively labeled CaCl2 (0.6-0.75 mu Ci (CaCl2)-Ca-45) was used for Ca2+ transport monitoring. The results revealed that in the presence of ER antagonist 7 alpha, 17 beta-[9[(4,4,5,5,5-pentafluoropentyl) sulfinyl] nonyl] estra-1,3,5( 10)-triene-3,17-diol (ICI 182,780) (1 mu mol/L), the inhibitory effect of estradiol on mitochondrial Ca2+ efflux was more than 60% decreased, suggesting the involvement of ER in this mode of estradiol neuromodulatory action. When particular contributions of ER alpha and ER beta were tested, it was found that ER beta agonist 2,3-bis(4-hydroxy phenyl)-propionitrile (10 nmol/L) inhibited Ca2+ efflux more than 20%, while the inhibition with ER alpha agonist 4,4, 4-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (10 nmol/L) was about 10%, both compared to the control. Both agonists demonstrated attenuation of Ca2+ efflux decrease in the presence of mitochondrial Na+/Ca2+ exchanger antagonist 7-chloro-5-(2-chlorophenyl)-1,5-dihyhdro-4,1-benzothiazepin-2(3H)-one (10 mu mol/L), showing interference with the inhibitory action of that agent. Our results strongly indicate ERs as the mediators of estradiol-induced mitochondrial Ca2+ efflux inhibition in rat caudate nucleus and brain stem synaptosomes.", journal = "Turkish Journal of Biology", title = "Estradiol receptors mediate estradiol-induced inhibition of mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem", volume = "39", number = "2", pages = "328-334", doi = "10.3906/biy-1408-62" }
Petrović, S., Milošević, M., Ristic-Medic, D., Velickovic, N., Drakulić, D. R., Grković, I.,& Horvat, A.. (2015). Estradiol receptors mediate estradiol-induced inhibition of mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem. in Turkish Journal of Biology, 39(2), 328-334. https://doi.org/10.3906/biy-1408-62
Petrović S, Milošević M, Ristic-Medic D, Velickovic N, Drakulić DR, Grković I, Horvat A. Estradiol receptors mediate estradiol-induced inhibition of mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem. in Turkish Journal of Biology. 2015;39(2):328-334. doi:10.3906/biy-1408-62 .
Petrović, Snježana, Milošević, Maja, Ristic-Medic, Danijela, Velickovic, Natasa, Drakulić, Dunja R., Grković, Ivana, Horvat, Anica, "Estradiol receptors mediate estradiol-induced inhibition of mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem" in Turkish Journal of Biology, 39, no. 2 (2015):328-334, https://doi.org/10.3906/biy-1408-62 . .