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1

Gene expression profiles for mitochondria sirtuins and poly(ADP-ribose) polymerases in amyloid Beta toxicity

100%
Strosznajder R., Wencel P.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Sirtuins (SIRTs) and poly(ADPribose) polymerases (PARPs) are NAD dependent enzymes engaged in the regulation of energy metabolism, transcription, DNA replication and repair. SIRTs type III histone deacetylases (HDAC) target histone and many other proteins in nucleus, cytoplasm and mitochondria. PARP-1 is responsible for over 90% of poly (ADPribosylation) in the brain. However, the role of these NAD dependent enzymes in neurodegeneration /neuroprotection is till now not fully elucidated. In many neurodegenerative disorders metabolism of amyloid precursor protein (APP) is altered, amyloid beta (Aβ) is released and NAD dependent metabolic pathways are affected. This study focused on gene expression profiles for SIRTs and PARPs and on their functional relationship in cells survival/death under Aβ toxicity. METHODS: PC-12 cells after exposition on exogenous Aβ1-42 oligomers (ABO -1 mM, 24 h) were used. Moreover, the effect of endogenously liberated Aβ in PC12 cells transfected with human gene for APP wild type (APPwt) and bearing Swedish mutation (APPsw) was investigated. The both served as experimental models. RESULTS: Our data indicated that ABO suppressed alpha secretase and enhanced gene expression for beta and gamma secretases. Moreover, ABO upregulated the gene expression for PARP-1, PARP-2 and SIRT4 which is responsible for monoADPribosylation of several mitochondrial proteins. The endogenously liberated Aβ in APPwt cells upregulated gene expression for PARP-1, -2 and decreased for SIRT5. In APPsw cells activation of genes for PARP -1,-2,-9 and for SIRT3 was observed. In our previous study we observed significant suppression of PARP activity in APPsw cells. CONCLUSIONS: These results suggest that NAD is not used by PARPs in APPsw cells and it may be available for Sirt3 which is involved in regulation of antioxidative enzymes. The functional interactions between these NAD dependent enzymes may play crucial role in regulation of cell survival under Aβ peptide toxicity. Supported by MRC.
2

Występowanie zakażeń herpeswirusem gołębi (CoHV -1) w kraju

100%
Wozniakowski G., Wencel P.
Polskie Drobiarstwo
|
2014
|
tom 22
|
nr 08
3

Występowanie zakażeń herpeswirusem gołebi (CoHV -1) w kraju

100%
Wozniakowski G., Wencel P.
Polskie Drobiarstwo
|
2014
|
tom 22
|
nr 08
4

Choroby wirusowe układu oddechowego ptaków

81%
Tokarzewski S., Wencel P., Blachowski J.
Hodowca Drobiu
|
2011
|
nr 11
5

Fingolimod (FTY720 - modulator of sphingosine 1-phosphate receptors) alters genes expression of selected NADplus-dependent enzymes in an animal model of Alzheimer’s disease

81%
Wencel P., Jesko H., Strosznajder R. P.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
INTRODUCTION: Sirtuins (SIRTs) and poly(ADP-ribose) polymerases (PARPs) belong to the family of NAD+ ‑dependent enzymes. Both are involved in the regulation of energy homeostasis, cellular stress response, and DNA repair. Recent data suggest that alterations of bioactive sphingolipids level as well as SIRTs and PARPs may be involved in Alzheimer’s disease (AD) pathology, finally leading to the progression of disease. AIM(S): In this study, the effect of FTY720 administration on mRNA levels of SIRTs and PARP‑1 in an animal model of AD was examined. METHOD(S): 3‑, 6‑, and 12‑month‑old (3M, 6M, 12M) FVB/APP+ transgenic mice with London APP (V717I) mutation were used in this study. Mice without the mutation (APP- ) were used as the control. Animals received i.p. FTY720 (1mg/kg b.w.) or NaCl (vehicle) for 2 weeks. Brain cortex was isolated and qPCR methods were applied. RESULTS: A significant downregulation of Sirt1 mRNA levels in the cortex of 3M APP+ mice vs. APP- was observed. We also observed a tendency for a reduction of 6M Sirt3 and Sirt4 mRNA levels in APP+ mice. Administration of FTY720 increased mRNA levels of Sirt1 in 3M APP+ mice as well as Parp1, Sirt1, 3, 5 in 6M APP+ mice compared to APP+ mice treated with vehicle. Moreover, FTY720 elevated Parp1, Sirt1, and Sirt3 mRNA levels in 12M APP+ mice. CONCLUSIONS: The results of our study revealed a potential link between bioactive sphingolipids and NAD+ ‑dependent enzymes. These results may also indicate an FTY720-modulatory role in SIRTs and PARPs gene expression and may offer a useful tool in the therapeutic strategy of neurodegenerative disorders. FTY720, through the activation of mitochondrial sirtuins (Sirt3,5), may improve anti-oxidative defense and protect cells against oxidative stress evoked by amyloid beta toxicity. Moreover, through activation of Sirt1 and Parp1 gene expression, FTY720 may enhance DNA repair processes. FINANCIAL SUPPORT: Supported by the National Science Centre grant no. NCN 2014/15/B/NZ3/01049 and Mossakowski MRC PAS statutory theme no.7.
6

The effect of a sphingosine-1-phosphate receptors modulator on the transcriptional profile of genes linked to glutamate homeostasis in the sporadic and genetic animal models of Alzheimer’s disease

71%
Wencel P., Sulkowski G., Dabrowska-Bouta B., Strosznajder R. P., Struzynska L.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
INTRODUCTION: Alzheimer’s disease (AD) is neurodegenerative disorder characterized by progressive memory impairment and cognitive failure which leads to dementia in aged population. Lots of data indicate glutamate-mediated neurotoxicity as a one of the pathomechanisms responsible for neuronal cell death during the course of AD. AIM(S): In this study, we examined the effect of fingolimod (FTY720‑modulator of sphingosine‑1‑phosphate receptors) on the transcription of genes involved in the homeostasis of glutamatergic system in animal models of AD. METHOD(S): 3‑ and 12‑month‑old (3M, 12M) FVB/ APP+ transgenic mice with the London (V717I) APP mutation were used in this study. Mice without the mutation (APP- ) were used as a control. The sporadic AD model was induced by injection of streptozotocin (STZ, icv. 2,5 mg/kg b.w.) in ACSF (vehicle) to 3M C57BL/6 mice. Animals received FTY720 (1mg/kg b.w.) or NaCl (vehicle) for 2 weeks. Brain cortex was isolated and qPCR methods were applied. RESULTS: Our results indicate a different model‑dependent profile of changes in gene expression. We observed significant upregulation of Slc17a7(VGluT1), Grin1(- GluN1), and Grm3 (mGluR3) gene expression in APP+ 12M mice. A significant elevation of Gria1(GluR‑1) and Grin1 (GluN1) mRNA levels with an accompanying decrease of Slc17a8 (VGluT3) and Grm5 (mGluR5) was observed in STZ mice. The administration of FTY720 led to a decrease in Gria2 (GluR-2) and Grm3 mRNA levels, as well as, an elevation of Slc1a3 (GluT‑1), Slc17a7, and Slc17a8 mRNA in STZ mice compared to appropriate controls. Transcriptional changes in vesicular glutamate transporters (Slc17a7 and Slc17a8) as well as glutamate receptors genes (Grin1, Gria1, Grm3,5) suggest that they may be involved in the mechanisms leading to AD. CONCLUSIONS: FTY720 may potentially modulate the expression of genes involved in homeostasis of the glutamatergic system in the model of sporadic AD. FINANCIAL SUPPORT: Supported by the National Science Centre grant no. NCN2014/15/B/NZ3/01049
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