Desanka Milanovic

Publications (7)22.59 Total impact

• Source

  Available from: Sabera Ruzdijic

  Article: Caloric restriction suppresses microglial activation and prevents neuroapoptosis following cortical injury in rats.

  Natasa Loncarevic-Vasiljkovic, Vesna Pesic, Smilja Todorovic, Jelena Popic, Kosara Smiljanic, Desanka Milanovic, Sabera Ruzdijic, Selma Kanazir
  [show abstract] [hide abstract]
  ABSTRACT: Traumatic brain injury (TBI) is a widespread cause of death and a major source of adult disability. Subsequent pathological events occurring in the brain after TBI, referred to as secondary injury, continue to damage surrounding tissue resulting in substantial neuronal loss. One of the hallmarks of the secondary injury process is microglial activation resulting in increased cytokine production. Notwithstanding that recent studies demonstrated that caloric restriction (CR) lasting several months prior to an acute TBI exhibits neuroprotective properties, understanding how exactly CR influences secondary injury is still unclear. The goal of the present study was to examine whether CR (50% of daily food intake for 3 months) alleviates the effects of secondary injury on neuronal loss following cortical stab injury (CSI). To this end, we examined the effects of CR on the microglial activation, tumor necrosis factor-α (TNF-α) and caspase-3 expression in the ipsilateral (injured) cortex of the adult rats during the recovery period (from 2 to 28 days) after injury. Our results demonstrate that CR prior to CSI suppresses microglial activation, induction of TNF-α and caspase-3, as well as neurodegeneration following injury. These results indicate that CR strongly attenuates the effects of secondary injury, thus suggesting that CR may increase the successful outcome following TBI.
  PLoS ONE 01/2012; 7(5):e37215. · 4.09 Impact Factor
• Source

  Available from: Sabera Ruzdijic

  Article: Propofol-induced changes in neurotrophic signaling in the developing nervous system in vivo.

  Jelena Popic, Vesna Pesic, Desanka Milanovic, Smilja Todorovic, Selma Kanazir, Vesna Jevtovic-Todorovic, Sabera Ruzdijic
  [show abstract] [hide abstract]
  ABSTRACT: Several studies have revealed a role for neurotrophins in anesthesia-induced neurotoxicity in the developing brain. In this study we monitored the spatial and temporal expression of neurotrophic signaling molecules in the brain of 14-day-old (PND14) Wistar rats after the application of a single propofol dose (25 mg/kg i.p). The structures of interest were the cortex and thalamus as the primary areas of anesthetic actions. Changes of the protein levels of the brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), their activated receptors tropomyosin-related kinase (TrkA and TrkB) and downstream kinases Akt and the extracellular signal regulated kinase (ERK) were assessed by Western immunoblot analysis at different time points during the first 24 h after the treatment, as well as the expression of cleaved caspase-3 fragment. Fluoro-Jade B staining was used to follow the appearance of degenerating neurons. The obtained results show that the treatment caused marked alterations in levels of the examined neurotrophins, their receptors and downstream effector kinases. However, these changes were not associated with increased neurodegeneration in either the cortex or the thalamus. These results indicate that in the brain of PND14 rats, the interaction between Akt/ERK signaling might be one of important part of endogenous defense mechanisms, which the developing brain utilizes to protect itself from potential anesthesia-induced damage. Elucidation of the underlying molecular mechanisms will improve our understanding of the age-dependent component of anesthesia-induced neurotoxicity.
  PLoS ONE 01/2012; 7(4):e34396. · 4.09 Impact Factor
• Article: Antiproliferative effect of 13-cis-retinoic acid is associated with granulocyte differentiation and decrease in cyclin B1 and Bcl-2 protein levels in G0/G1 arrested HL-60 cells.

  Ana Vuletic, Gordana Konjevic, Desanka Milanovic, Sabera Ruzdijic, Vladimir Jurisic
  [show abstract] [hide abstract]
  ABSTRACT: Retinoic acid (RA), similar to specific growth factors, can induce differentiation of proliferating promyelocytic precursors into terminally differentiated granulocytes, although little is known about effects of its 13-cis isomer on promyelocytic leukemia (PML). In this study we demonstrate that 13-cis-RA has a dose and time-dependent antiproliferative effect on HL-60 PML cell line, that it induces cell accumulation in resting G0/G1 phase of the cell cycle followed by an increase in CD11b granulocyte differentiation antigen expression. The obtained increase in the percentage of HL-60 cells in G0/G1 phase and complementary decrease in S phase of the cell cycle are accompanied by a decrease in the expression of cell cycle regulatory molecule cyclin B1. We also show the induction of interferon regulatory factor-1 (IRF-1) transcription that can, also, to some extent contribute to the antiproliferative effect of 13-cis-RA. Furthermore, down-regulation of Bcl-2 protein expression in 13-cis-RA treated HL-60 cells may contribute to sensitivity to apoptosis of growth arrested HL-60 promyelocytic cells.
  Pathology & Oncology Research 09/2010; 16(3):393-401. · 1.37 Impact Factor
• Article: Regional and temporal profiles of calpain and caspase-3 activities in postnatal rat brain following repeated propofol administration.

  Desanka Milanovic, Jelena Popic, Vesna Pesic, Natasa Loncarevic-Vasiljkovic, Selma Kanazir, Vesna Jevtovic-Todorovic, Sabera Ruzdijic
  [show abstract] [hide abstract]
  ABSTRACT: Exposure of newborn rats to a variety of anesthetics has been shown to induce apoptotic neurodegeneration in the developing brain. We investigated the effect of the general anesthetic propofol on the brain of 7-day-old (P7) Wistar rats during the peak of synaptic growth. Caspase and calpain protease families most likely participate in neuronal cell death. Our objective was to examine regional and temporal patterns of caspase-3 and calpain activity following repeated propofol administration (20 mg/kg). P7 rats were exposed for 2, 4 or 6 h to propofol and killed 0, 4, 16 and 24 h after exposure. Relative caspase-3 and calpain activities were estimated by Western blot analysis of the proteolytic cleavage products of α-II-spectrin, protein kinase C and poly(ADP-ribose) polymerase 1. Caspase-3 activity and expression displayed a biphasic pattern of activation. Calpain activity changed in a region- and time-specific manner that was distinct from that observed for caspase-3. The time profile of calpain activity exhibited substrate specificity. Fluoro-Jade B staining revealed an immediate neurodegenerative response that was in direct relationship to the duration of anesthesia in the cortex and inversely related to the duration of anesthesia in the thalamus. At later post-treatment intervals, dead neurons were detected only in the thalamus 24 h following the 6-hour propofol exposure. Strong caspase-3 expression that was detected at 24 h was not followed by cell death after 2- and 4-hour exposures to propofol. These results revealed complex patterns of caspase-3 and calpain activities following prolonged propofol anesthesia and suggest that both are a manifestation of propofol neurotoxicity at a critical developmental stage.
  Developmental Neuroscience 01/2010; 32(4):288-301. · 3.63 Impact Factor
• Article: Enhancement of AP-1 DNA-binding activity during amphetamine- and phencyclidine-mediated behaviour in rats.

  Desanka Milanovic, Vesna Pesic, Ljubisav Rakic, Selma Kanazir, Sabera Ruzdijic
  [show abstract] [hide abstract]
  ABSTRACT: Amphetamine (AMPH) and phencyclidine (PCP) induce a variety of behavioural and synaptic changes in the brain, many of which are believed to involve the regulation of gene expression. In this study, we examined the effects of AMPH (5mg/kg), PCP (5mg/kg) and their combination (5mg/kg each) on rat motor activity as well as on the activation of the AP-1 transcription factor in rat brains. AMPH administration, followed by PCP, led to a statistically significant elevation of locomotor activity. It was found that the behavioural response of rats was more pronounced when the two drugs were administered together. The electrophoretic mobility shift assay (EMSA) revealed a significant increase in AP-1-binding activity after treatments with AMPH, PCP or their combination. Super shift/shift inhibition analysis demonstrated the presence of c-Fos and c-Jun protein families in the transcriptional complex bound to AP-1 sequences. Further, our results suggest that the enhanced behavioural changes after AMPH and PCP administration were associated with increased expression of AP-1 proteins (Fos and Jun) in the cortex, striatum and hippocampus and that their binding to AP-1 sites on the DNA contributes to long-term changes in rat brain.
  Neuropharmacology 07/2006; 50(8):924-33. · 4.81 Impact Factor
• Source

  Available from: Miroslava T Vujcic

  Article: Effects of age and dexamethasone treatment on glucocorticoid response element and activating protein-1 binding activity in rat brain.

  Natasa Terzic, Miroslava Vujcic, Aleksandra Ristic-Fira, Marija Krstic-Demonacos, Desanka Milanovic, Dusan T Kanazir, Sabera Ruzdijic
  [show abstract] [hide abstract]
  ABSTRACT: The effect of dexamethasone (DEX) on glucocorticoid receptor (GR)-mediated gene expression was examined in the brain of young and aged rats. Electrophoretic mobility shift assays showed that DEX treatment led to an increase of glucocorticoid response element (GRE) binding activity in aged rats, whereas in young animals GRE binding activity was decreased. Western blot analysis and reverse transcriptase polymerase chain reaction confirmed that, in aged animals, the GR mRNA and the GR protein levels were increased on DEX treatment. The binding activity of GRE activating protein-1 (AP-1) site and cross-competition analysis demonstrated specific pattern of expression during the ageing and DEX treatment, suggesting that GR modulates the activity of transcription factors AP-1 (Fos/Jun proteins) through protein-protein interaction. On the basis of these results, it can be concluded that the composition of transcriptional complexes that bind to GRE and AP-1 regulatory elements changes upon DEX treatment in an age-specific manner.
  The Journals of Gerontology Series A Biological Sciences and Medical Sciences 05/2003; 58(4):297-303. · 4.60 Impact Factor
• Article: Effects of Age and Dexamethasone Treatment on Glucocorticoid Response Element and Activating Protein-1 Binding Activity in Rat Brain

  Natasa Terzic, Miroslava Vujcic, Aleksandra Ristic-Fira, Marija Krstic-Demonacos, Desanka Milanovic, Dusan T. Kanazir, Sabera Ruzdijic
  [show abstract] [hide abstract]
  ABSTRACT: The effect of dexamethasone (DEX) on glucocorticoid receptor (GR)-mediated gene expression was examined in the brain of young and aged rats. Electrophoretic mobility shift assays showed that DEX treatment led to an increase of glucocorticoid response element (GRE) binding activity in aged rats, whereas in young animals GRE binding activity was decreased. Western blot analysis and reverse transcriptase polymerase chain reaction confirmed that, in aged animals, the GR mRNA and the GR protein levels were increased on DEX treatment. The binding activity of GRE activating protein-1 (AP-1) site and cross-competition analysis demonstrated specific pattern of expression during the ageing and DEX treatment, suggesting that GR modulates the activity of transcription factors AP-1 (Fos/Jun proteins) through protein–protein interaction. On the basis of these results, it can be concluded that the composition of transcriptional complexes that bind to GRE and AP-1 regulatory elements changes upon DEX treatment in an age-specific manner.
  Journal of Gerontology 01/2003; 58a(4):297-303.