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1

Up-regulated glial TrkA may mediate neuroprotective effects of NGF-releasing, anti-MBP CD4 T cells administered into trimethyltin intoxicated rats

100%
Kurkowska-Jastrzebska I., Zaremba M., Joniec L., Figiel I., Lukasiuk E., Czlonkowska A., Oderfeld-Nowak B.
Acta Neurobiologiae Experimentalis
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2006
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tom 66
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nr 4
2

Age and gender influence on astrocyte activation in model of Parkinson's disease (PD)

100%
Ciesielska A., Joniec L., Przybylkowski A., Kurkowska-Jastrzebska I., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
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2005
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tom 65
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nr 3
3

Inhibitory effects of 17beta-estradiol on production of both molecular and cellular factors in neuroinflammatory reaction in model of Parkinson's disease

84%
Ciesielska A., Joniec L., Cudna A., Kurkowska-Jastrzebska L., Sznejder A., Zaremba N., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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nr 3
The neuroprotective action of 17β-estradiol (E2) against 1-methyl4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown in both female and male mice, however the exact mechanisms of that phenomenon remain obscured. We studied the chronic effects of E2 (0.25 mg per pellet, 21-days release) administered 7 days prior (Experiment 1) to or 3 days after (Experiment 2) MPTP intoxication (40 mg/kg, i.p.) in C57BL aged male mice on neurodegenerative and infl ammatory processes in nigrostriatal pathway. We estimated striatal: tyrosine hydroxylase (TH), glial fi brillary acidic protein (GFAP) content (Western blotting); cytokines (TNFα, TGFβ1, IFNγ), trophic factor (GDNF) gene expression (RT-PCR); CD4+ and CD8+ cells infl ux (immunohistochemistry) at 1, 7, 21 (Exp. 1) and 7, 21 (Exp. 2) days post intoxication. E2 exerted a neuroprotective effect upon nigrostriatal system when administered prior but also when administered after intoxication (E2 attenuated the MPTP-induced loss of TH). E2 also decreased the GFAP content. MPTP caused a rapid increase of TGFβ1, TNFα and IFNγ. Pre-treatment with E2 decreased the early expression of TGFβ1 and IFNγ but failed to suppress the MPTP-induced increase of TNFα. E2 pre-treatment also induced an increase of the GDNF and CD4+ cells infl ux to the injured brain areas but decreased the CD8+ cells infi ltration. The neuroprotective effects of E2 indicated in MPTP model might mediate through a modulation of neuroinfl ammatory reaction in lesioned nigrostriatal system.
4

The molecular and behavioral changes in the long-term observations in mice model of Parkinson's disease

84%
Zaremba M., Joniec L., Piechal A., Pyrzanowska J., Kurkowska-Jastrzebska L., Ciesielska A., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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nr 3
The pathogenesis of non-motor symptoms in Parkinson’s disease (PD) is complex and not fully understood, but is believed to be related to the widespread nature of dopaminergic dysfunction involving structures beyond the substantia nigra. Therefore we’ve also focused in our experiments on specifi c brain regions (e.g. hippocampus and prefrontal cortex) critically involved in spatial learning and memory processes. One year old C57/BL male mice received 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrindine (MPTP) 40 mg/kg, and control group received 0.9 % NaCl. To evaluate spatial learning and memory abilities, the Morris water maze (WM) behavioral test was provided after 6 months from the intoxication. The brain concentration of monoamines: dopamine (DA), noradrenaline (NA), 5 – hydroxytryptamine (5-HT) and amino acid: glutamate (Glu) were determined by using high – performance liquid chromatography (HPLC). Statistical signifi cances differences in monoamines levels between groups were noticed in hippocampus (NA, DA content) and prefrontal cortex (NA content). We didn’t notice signifi cant differences in the WM test parameters between MPTP and the control animals. Correlation between the results of the behavioral testing in the probe trial and the level of monoamines were calculated. Swim distance to reach the hidden platform was negatively correlated with NA level in the hippocampus (rp=−0.62, P<0.05). There is need for a further investigation to confi rm the role for NA in spatial memories.
5

Neuroprotective effects of AAV2-h1L-10 in mouse model of Parkinson's disease

84%
Joniec L., Ciesielska A., Gladka A., Cudna A., Zaremba M., Kurkowska-Jastrzebska L., Hadaczek P., Bankiewicz H., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Parkinson’s disease (PD) is a neurodegenerative disorder which is characterized by abnormal loss of nigrostriatal dopamine (DA) neurons, accompanied by DA defi ciency in the striatum. The pathomechanism by which DA neurons degenerate is still unknown, however, there is increasing evidence that is possible immunological mechanisms involvement in the etiopathogenesis of PD. The aim of the present study was to examine the effect of an adeno-associated viral type-2 (AAV2) vector containing human interleukin-10 (hIL-10) gene on dopaminergic system restoration in the murine model of PD induced by by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Male C57BL/6 mice 12 months-old were used in this study. MPTP was injected in four intraperitoneal injections at 1-h intervals. AAV2-hIL-10 vector was bilaterally administered into striatum at 14, 21 or 28 days prior to MPTP intoxication. Animals were sacrifi ced at 7 days following MPTP injection. Striatal DA, DOPAC, HVA concentrations were quantifi ed by HPLC method; tyrosine hydroxylase (TH) mRNA expression was measured by RT-PCR method. MPTP treatment dramatically decreased DA concentration, signifi cantly decreased TH mRNA gene expression. AAV2-hIL-10 exerted a neuroprotective effect upon dopaminergic system (lower decrease in DA concentration). Additionally, viral vector administration prevented depletion of TH mRNA expression induced by MPTP. Our data suggest that AAV2-hIL-10 may play a neuroprotective role in MPTP mouse model of PD.
6

Effect of AAF-2-h1L-10 on immune response following toxic degeneration caused by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in micep.345

84%
Joniec L., Ciesielska A., Gladka A., Schwenkgrub J., Sznejder A., Cudna A., Hadaczek P., Bankiewicz K., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Interleukine 10 (IL-10) – an antiinfl ammatory cytokine produced by lymphocytes and mononuclear phagocytes including microglia. IL10 modulates the biological activities of immune cells resulting in a decreased production of pro-infl ammatory mediators including cytokines, chemokines and adhesion molecules. The aim of the present study was to examine the effect of an adeno-associated viral type-2 (AAV2) vector containing human interleukin-10 (hIL-10) gene to evaluation of immune response to the AAV2-hIL-10 (measured as IFN-γ, GFAP and TGFβ mRNA expression) in the murine model of Parkinson’s disease (PD) induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Male C57BL/6 mice 12 months-old were used in this study. MPTP (40 mg/kg) was injected in four intraperitoneal injections at 1-h intervals. AAV2-hIL-10 vector was bilaterally administered into striatum at 14, 21 or 28 days prior to MPTP intoxication. Animals were sacrifi ced by spinal cords dislocation at 7 days following MPTP injection. TGFβ, IFN-γ and GFAP mRNA expression was examined by RT-PCR method. MPTP treatment signifi cantly increased IFN-γ mRNA expression. AAV2-hIL-10 administration strongly increased IFN-γ as well as TGFβ and GFAP (21 and 28 day) gene expression compared to control and MPTP group. Our results point to the necessity of the reinterpretation of the role of the infl ammatory reaction in nerodegenerative processes
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