TY  - JOUR
AU  - Filipović, Dragana
AU  - Zlatković, Jelena
AU  - Pavicevic, Ivan
AU  - Mandic, Ljuba
AU  - Demajo, Miroslav
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4360
AB  - The c-Jun NH2-terminal kinases (JNKs) are important stress-responsive kinases. They regulate cellular activities by sequential phosphorylation and activation through a mitogen-activated protein kinase cascade, whereas JNKs activation is altered in response to various stressors. In the present study, we used immunoblotting to assess the effect of 21 day of social isolation as the chronic stressor, either sole and in combination with 2 h of acute immobilization or cold (4A degrees C) stress on circulating corticosterone level and phosphorylation status of p46 (phospho-p46/total p46) and p54 (phospho-p54/total p54) JNK isoforms in the cytosolic and nuclear fraction of the prefrontal cortex and hippocampus of male Wistar rats. Also, the phosphorylation status of JNK nuclear down-stream target c-Jun (p-c-Jun/c-Jun) on Ser63 was examined. Both acute stressors with elevated CORT levels led to increased phosphorylation status of cytosolic p54 JNK isoforms but not p46 JNK isoforms only in the hippocampus and no change in phosphorylation status of c-jun in both brain regions. Chronic isolation with unaltered CORT level and reduced responsiveness to novel acute stressors, led to unchanged or reduced phosphorylation status of p46 and p54 JNK isoforms in both fractions and both brain regions, whereas the decrease of c-Jun phosphorylation status was found only in the prefrontal cortex. Our results suggest that compromised JNKs activation following chronic isolation may lead to interruption of JNK signaling, which could be related with neuropsychiatric disorders such as depression or long-lasting neuronal remodeling.
T2  - Journal of Neural Transmission
T1  - Chronic isolation stress compromises JNK/c-Jun signaling in rat brain
VL  - 119
IS  - 11
SP  - 1275
EP  - 1284
DO  - 10.1007/s00702-012-0776-0
ER  - 

@article{
author = "Filipović, Dragana and Zlatković, Jelena and Pavicevic, Ivan and Mandic, Ljuba and Demajo, Miroslav",
year = "2012",
abstract = "The c-Jun NH2-terminal kinases (JNKs) are important stress-responsive kinases. They regulate cellular activities by sequential phosphorylation and activation through a mitogen-activated protein kinase cascade, whereas JNKs activation is altered in response to various stressors. In the present study, we used immunoblotting to assess the effect of 21 day of social isolation as the chronic stressor, either sole and in combination with 2 h of acute immobilization or cold (4A degrees C) stress on circulating corticosterone level and phosphorylation status of p46 (phospho-p46/total p46) and p54 (phospho-p54/total p54) JNK isoforms in the cytosolic and nuclear fraction of the prefrontal cortex and hippocampus of male Wistar rats. Also, the phosphorylation status of JNK nuclear down-stream target c-Jun (p-c-Jun/c-Jun) on Ser63 was examined. Both acute stressors with elevated CORT levels led to increased phosphorylation status of cytosolic p54 JNK isoforms but not p46 JNK isoforms only in the hippocampus and no change in phosphorylation status of c-jun in both brain regions. Chronic isolation with unaltered CORT level and reduced responsiveness to novel acute stressors, led to unchanged or reduced phosphorylation status of p46 and p54 JNK isoforms in both fractions and both brain regions, whereas the decrease of c-Jun phosphorylation status was found only in the prefrontal cortex. Our results suggest that compromised JNKs activation following chronic isolation may lead to interruption of JNK signaling, which could be related with neuropsychiatric disorders such as depression or long-lasting neuronal remodeling.",
journal = "Journal of Neural Transmission",
title = "Chronic isolation stress compromises JNK/c-Jun signaling in rat brain",
volume = "119",
number = "11",
pages = "1275-1284",
doi = "10.1007/s00702-012-0776-0"
}

Filipović, D., Zlatković, J., Pavicevic, I., Mandic, L.,& Demajo, M.. (2012). Chronic isolation stress compromises JNK/c-Jun signaling in rat brain. in Journal of Neural Transmission, 119(11), 1275-1284.
https://doi.org/10.1007/s00702-012-0776-0

Filipović D, Zlatković J, Pavicevic I, Mandic L, Demajo M. Chronic isolation stress compromises JNK/c-Jun signaling in rat brain. in Journal of Neural Transmission. 2012;119(11):1275-1284.
doi:10.1007/s00702-012-0776-0 .

Filipović, Dragana, Zlatković, Jelena, Pavicevic, Ivan, Mandic, Ljuba, Demajo, Miroslav, "Chronic isolation stress compromises JNK/c-Jun signaling in rat brain" in Journal of Neural Transmission, 119, no. 11 (2012):1275-1284,
https://doi.org/10.1007/s00702-012-0776-0 . .

TY  - JOUR
AU  - Filipović, Dragana
AU  - Mandic, Ljuba M.
AU  - Kanazir, Dušan T.
AU  - Pajović, Snežana B.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/3979
AB  - Cellular protection against oxidative stress is afforded by the enzyme superoxide dismutase (SOD). In this study, the protein levels of copper-zinc SOD (CuZnSOD) in the cytosolic and nuclear fraction, manganese SOD (MnSOD) in the mitochondrial, and cytosolic fraction and cytochrome c (cyt c) in the liver of male rats exposed to 2 h of acute immobilization (IM) or Cold stress, 21 days chronic isolation or their combinations (chronic/acute stress) were examined. The serum corticosterone (CORT) level was measured, as an indicator of stress stimuli. Both acute stressors with elevated CORT levels caused a decrease of mitochondrial MnSOD, while acute IM resulted in redistribution of the CuZnSOD protein level between the cytosolic and nuclear fraction. Chronic isolation, during which the CORT level was close to control value, resulted in an increase of cytosolic CuZnSOD, whereas a decrease of MnSOD in mitochondrial and its corresponding increase in cytosol fraction was found. In both combined stress regimes, an increase of the CuZnSOD and MnSOD levels in the cytosolic fraction was recorded whereby increase of the CORT level was observed only in the chronic isolation followed by acute IM. The data indicate that acute and/or chronic stress models have different degrees of influence on serum CORT and SOD subcellular protein levels. Increased cytosolic CuZnSOD protein level under chronic isolation suggests that state of oxidative stress may also exist under CORT level similar to the basal value. The presence of MnSOD and cyt c in the cytosolic fraction could serve as useful parameters for mitochondrial dysfunction.
T2  - Molecular and Cellular Biochemistry
T1  - Acute and/or chronic stress models modulate CuZnSOD and MnSOD protein expression in rat liver
VL  - 338
IS  - 1-2
SP  - 167
EP  - 174
DO  - 10.1007/s11010-009-0350-8
ER  - 

@article{
author = "Filipović, Dragana and Mandic, Ljuba M. and Kanazir, Dušan T. and Pajović, Snežana B.",
year = "2010",
abstract = "Cellular protection against oxidative stress is afforded by the enzyme superoxide dismutase (SOD). In this study, the protein levels of copper-zinc SOD (CuZnSOD) in the cytosolic and nuclear fraction, manganese SOD (MnSOD) in the mitochondrial, and cytosolic fraction and cytochrome c (cyt c) in the liver of male rats exposed to 2 h of acute immobilization (IM) or Cold stress, 21 days chronic isolation or their combinations (chronic/acute stress) were examined. The serum corticosterone (CORT) level was measured, as an indicator of stress stimuli. Both acute stressors with elevated CORT levels caused a decrease of mitochondrial MnSOD, while acute IM resulted in redistribution of the CuZnSOD protein level between the cytosolic and nuclear fraction. Chronic isolation, during which the CORT level was close to control value, resulted in an increase of cytosolic CuZnSOD, whereas a decrease of MnSOD in mitochondrial and its corresponding increase in cytosol fraction was found. In both combined stress regimes, an increase of the CuZnSOD and MnSOD levels in the cytosolic fraction was recorded whereby increase of the CORT level was observed only in the chronic isolation followed by acute IM. The data indicate that acute and/or chronic stress models have different degrees of influence on serum CORT and SOD subcellular protein levels. Increased cytosolic CuZnSOD protein level under chronic isolation suggests that state of oxidative stress may also exist under CORT level similar to the basal value. The presence of MnSOD and cyt c in the cytosolic fraction could serve as useful parameters for mitochondrial dysfunction.",
journal = "Molecular and Cellular Biochemistry",
title = "Acute and/or chronic stress models modulate CuZnSOD and MnSOD protein expression in rat liver",
volume = "338",
number = "1-2",
pages = "167-174",
doi = "10.1007/s11010-009-0350-8"
}

Filipović, D., Mandic, L. M., Kanazir, D. T.,& Pajović, S. B.. (2010). Acute and/or chronic stress models modulate CuZnSOD and MnSOD protein expression in rat liver. in Molecular and Cellular Biochemistry, 338(1-2), 167-174.
https://doi.org/10.1007/s11010-009-0350-8

Filipović D, Mandic LM, Kanazir DT, Pajović SB. Acute and/or chronic stress models modulate CuZnSOD and MnSOD protein expression in rat liver. in Molecular and Cellular Biochemistry. 2010;338(1-2):167-174.
doi:10.1007/s11010-009-0350-8 .

Filipović, Dragana, Mandic, Ljuba M., Kanazir, Dušan T., Pajović, Snežana B., "Acute and/or chronic stress models modulate CuZnSOD and MnSOD protein expression in rat liver" in Molecular and Cellular Biochemistry, 338, no. 1-2 (2010):167-174,
https://doi.org/10.1007/s11010-009-0350-8 . .