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1

The association between maternal immune activation and mitochondrial failure in adulthood: relevance to neurodevelopmental disorders

100%
Cieslik M., Adamczyk A.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
Evidence suggests that maternal immune activation (MIA) during pregnancy is a risk factor for neurodevelopmental disturbances including autism spectrum disorders (ASDs). Animal models support this linkage and demonstrate that MIA in rodents leads to behavioral alterations in offspring that are characteristic of autism. However, the mechanism by which MIA causes long‑term behavioral deficits is unknown. Investigation of the links between maternal infection during pregnancy, mitochondrial dysfunction, and behavioral alterations in offspring. To induce MIA, pregnant Wistar rats were injected with lipopolysaccharide (LPS; 0.1mg/kg, intraperitoneally) on gestational day 9.5, a time point analogous to the first trimester of human gestation. Brains from adolescent offspring were evaluated for mitochondrial outcomes. Prenatal exposure to MIA led to anxiety and repetitive behavior. Adolescent offspring of MIA dams exhibited up-regulation of pro-inflammatory cytokines, oxidative stress, and disturbances in redox homoeostasis. Moreover, substantial mitochondrial abnormalities were observed. A significant decrease in mitochondrial membrane potential and changes in ATP production could be attributed to a downregulation of complex I and IV. Deregulated bioenergetics of mitochondria were accompanied by impaired mitochondrial dynamics, altered expression of fusion/fission machinery proteins including mitofusin 1 and 2 (Mfn1, Mfn2), Opa1, dynamin related protein‑1 (Drp1), and fission protein 1 (Fis1). We also demonstrated lower expression of the genes coding for PGC1α and TFAM (PPARGC1A and TFAM, respectively) that are responsible for mitochondrial biogenesis. MIA at early gestation leads to long-lasting effects on the mitochondrial bioenergetics, dynamics, and biogenesis in the offspring which can lead to synaptic dysfunction and behavioral abnormalities similar to ASD. FINANCIAL SUPPORT: Supported by the NSC grant 2016/23/D/NZ4/03572.
2

Leśne samochody patrolowo-gaśnicze

81%
Kolakowski B., Kaczmarowski J., Cieslik M.
Postępy Techniki w Leśnictwie
|
2018
|
tom 142
3

Role of lipoxygenases and poly(ADP-ribose) polymerase in amyloid beta cytotoxicity

81%
Cieslik M., Strosznajder J. B., Gajkowska B., Strosznajder R. P.
Acta Neurobiologiae Experimentalis
|
2011
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tom 71
|
nr 1
The roles of 12/15-lipoxygenase(s) (LOX), poly(ADP-ribose) polymerase (PARP-1) activity and mitochondrial apoptosis inducing factor (AIF) protein in the molecular processes evoked by amyloid β (Aβ) toxicity were investigated in PC12 cells that express either wild-type (APPwt) or double Swedish mutation (APPsw) forms of human Aβ precursor protein. Different levels of Aβ secretion characterize these cells. The results demonstrated a relationship between the Aβ levels and LOX protein expression and activity. High Aβ concentration in APPsw cells correlated with a significant increase in free radicals and LOX activation, which leads to translocation of p65/NF-κB into the nucleus. An increase in AIF expression in mitochondria was observed concurrently with inhibition of PARP-1 activity in the nuclear fraction of APPsw cells. AIF accumulation in mitochondria may be involved in adaptive/protective processes. However, inhibition of PARP-1 may be responsible for the disturbances in transcription and DNA repair as well as the degeneration of APP cells. Under conditions of increased nitrosative stress, evoked by the nitric oxide donor, sodium nitroprusside (SNP, 0.5 mM), 70-80 % of all cells types died after 24 h, significantly more in APPsw cells. There was no further significant change in mitochondrial AIF level and PARP-1 activity compared to corresponding nontreated with SNP cells. Only one exception was observed in PC12 control, where SNP significantly inhibits PARP-1 activity. Moreover, SNP significantly activated gene expression for 12/15-LOX in all types of investigated cells. Inhibitors of all LOX isoforms and specific inhibitor of 12-LOX enhanced the survival of cells that were subjected to SNP. We conclude that the LOX pathways may play a role in Aβ toxicity and in nitrosative-stress-induced cell death and that inhibition of these pathways offers novel protective strategies. Supported by MS&HE grant NN40113938 and MRC statutory theme No 7.
4

Sezon wystaw hodowlanych - już wkrótce (2)

81%
Klebaniuk R., Cieslik M., Rocki G., Olcha M.
Bydło
|
2014
|
nr 04
5

Żywienie zwierząt wystawowych

81%
Cieslik M., Klebaniuk R., Rocki G., Gozdz J.
Bydło
|
2014
|
nr 03
6

Żywienie zwierząt wystawowych (2)

81%
Cieslik M., Klebaniuk R., Rocki G., Gozdz J.
Bydło
|
2014
|
nr 04
7

Inhibitors of poly(ADP-ribose) polymerase protect hippocampal neurons against genotoxic stress via PI-3K/AKT regulated pathway and by suppression of AIF translocation

81%
Cieslik M., Jacewicz M., Strosznajder J. B.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 1
Poly(ADP-ribose)polymerase (PARP-1) plays a key role in DNA repair but its over activation has been proposed to be important in pathogenesis of brain ischemia and in neurodegenerative diseases. PARP catalyzes the conversion of bNAD+ to polymers of poly(ADP-ribose) (PAR) and is fully responsible for producing of PAR polymers during genotoxic stress. The last data indicated that PAR act at the mitochondria to induce cell death through stimulation of apoptosis inducing factor (AIF) release. However, the role of PAR in cell death seems to be complex and not fully elucidated. To better understand the role and relationship between AIF and PARP/PAR in death signaling the hippocampal neuronal (HT22) cells in culture were subjected to different concentration of DNA alkylating agent, 1-methyl-3-nitro-1-nitrosoguanidine (MNNG). The immunochemical and spectrophotometrical methods were applied. Consequently, HT22 cells treated with MNNG at 50ñ 500 mM demonstrated concentration dependent mitochondria failure and death. 24 h after 500 mM MNNG treatment only 15% of cells survive. PARP-1 inhibitors: 3-aminobenzamide (3AB) and PJ34 at 5 mM and 20 mM, respectively, protect most of the cells against MNNG induced death signaling. At lethal MNNG concentration PARP/PAR dependent AIF translocation from mitochondria is observed and the caspase independent death signaling is activated. Concomitantly PARP inhibitors affect the endogenous pathway regulated by PI-3K/AKT PKB/GSK-3 and infl uence the level of GSK-3β active form phosphorylated on Tyrosine 216. Summarizing our data indicated that inhibitors of PARP have positive effect on neuroprotective pathway regulated by PI-3K/AKT and on mitochondria function. Supported by Scientifi c Network of MS&HE No 28/E-32/SN0053/2007
8

Aktywne składniki roślinne - lekarstwo na globalne ocieplenie?

81%
Nowak A., Zmora P., Szczechowiak J., Cieslik M.
Ekonatura
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2012
|
nr 08
9

Sezon wystaw hodowlanych - już wkrótce (1)

81%
Klebaniuk R., Cieslik M., Rocki G., Olcha M.
Bydło
|
2014
|
nr 03
10

The molecular network between amyloid Beta peptide, sphingosine kinase and sirtuins in cell survival and death implication in Alzheimer's disease

81%
Strosznajder J., Czapski G., Cieslik M.
Acta Neurobiologiae Experimentalis
|
2015
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tom 75
|
nr Supl.
BACKGROUND AND AIMS: Deregulation of the sphingolipid metabolism plays an important role in the pathogenesis of Alzheimer’s disease (AD). Mitochondrial function and mitochondrial deacetylases, i.e. sirtuins (Sirt3,-4,-5), are also affected in AD. The aim of this study was to analyse the interaction between amyloid-β1-42 (Aβ1-42), sphingosine kinases (SphKs) and mitochondrial sirtuins in cell survival/death. METHODS: The spectrofluorometrical, immunochemical and QRT-PCR methods were applied. RESULTS: PC12 cells were subjected to Aβ1-42 oligomers and SphK inhibitor (SKI II) for 24–96 h.Aβ1-42 enhanced SphK1 expression and activity after 24 h, but down-regulated them after 96 h and had no effect on SphK2. Aβ1-42 and SKI II induced oxidative stress, disturbed the balance between pro- and anti-apoptotic proteins and evoked cell death. Simultaneously, up-regulation of anti-oxidative enzymes catalase and superoxide dismutase 2 occurred. Moreover, the total protein level of glycogen synthase kinase-3β (Gsk-3β) was reduced. Aβ1-42 significantly increased the level of mitochondrial proteins: AIF and Sirt3, -4, -5. Additional analysis demonstrated a significant role of p53 protein at very early stages of Aβ1-42 toxicity. However, during prolonged exposure to Aβ1-42, the activation of caspases, MEK/ERK, and alterations in mitochondrial permeability transition pores were also involved in mechanism responsible for cell death. Moreover, SphK product, sphingosine-1-phosphate (S1P), and Sirt activators and antioxidants, effectively prevented toxicity of Aβ1-42. CONCLUSIONS: Our data indicated that p53 protein and SphKs may be involved at early stage of molecular mechanisms of Aβ toxicity. We suggest the important role of interactions between Aβ peptide, SphKs and Sirts in pathomechanism of AD. The activation of S1P-dependent signalling and Sirts may offer a promising cytoprotective strategy. This study was supported by The National Science Centre Grant 2013/09/B/NZ3/01350 to J.B.S.
11

Dodatki energetyczne dla krów w początkowym okresie laktacji

81%
Klebaniuk R., Kochman G., Bakowski M., Cieslik M.
Hodowca Bydła
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2011
|
nr 10
12

Ceramide/sphingosine-1-phosphate in cellls survival and death: implication in Alzheimer’s disease

81%
Strosznajder R. P., Czubowicz K., Gassowska M., Cieslik M.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
Ceramide and sphingosine-1-phosphate (S1P) are very active sphingolipid messengers which play a crucial role in regulation of neuronal cells survival and death. Alternation of ceramide/S1P rheostat is related to several pathological disorders including Alzheimer’s disease. Ceramides are involved in cells proliferation, differentiation and apoptotic death, while S1P enhances cell proliferation and antagonizes apoptosis. S1P regulates cellular processes by binding to five specific G protein coupled-receptors (S1PR1-5). The aim of the study was to investigate the molecular processes of neuronal death evoked by ceramide and the role of S1P in neuroprotection. Our study indicated that ceramide enhanced significantly the level of free radicals and decreased neuronal cells (SHSY5Y) viability through inhibition of PI3-K/Akt pathway. Ceramide also decreased anti-apoptotic (Bcl-2) and increased pro-apoptotic (Bax, Hrk) gene expression. Exogenously added S1P increased the viability of cells through S1PR (1-3) receptors-dependent mechanism. S1P also increased Bcl-2 gene expression and decreased the gene expression of Hrk protein. Summarizing, our study indicated that the action of ceramide and S1P on mitochondria may control neuronal fate and may play a crucial role in neurodegeneration and neuroprotection.
13

Extracellular alpha-synuclein induces calpain-dependent overactivation of cyclin-dependent kinase 5 in PC12 cells

71%
Adamczyk A., Gasowska M., Wilkaniec A., Cieslik M., Czapski G. A.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
α-Synuclein (ASN) secreted from neurons into the extracellular space affects the homeostasis of neighboring cells, but the pathophysiology of extracellular ASN remains largely unknown. The aim of the present study was to analyze the role of cyclin dependent kinase 5 (Cdk5) in molecular mechanism of extracellular ASN toxicity. We found that exogenously applied ASN evoked apoptotic cell death in a significant population of dopaminergic PC12 cells. ASN induced rapid and long-lasting calcium influx and activation of calciumdependent enzymes, including caspase-3, nitric oxide synthase and calpain. ASN-induced calpain activation leads to cleavage of Cdk5 activator p35, and subsequently to formation of p25 and Cdk5 overactivation. Moreover, we showed that exposure of PC12 cells to ASN increased Cdk5 activity by enhancement of its phosphorylation at Tyr15. Calpeptin, an inhibitor of calpains, and inhibitors of Cdk5, Roscovitine and BML-259, prevented ASN-evoked apoptosis and cell death, indicating the involvement of Cdk5 in mechanism of ASN toxicity. Our data showed that alterations in calcium homeostasis and modulation of calcium-dependent enzymes by extracellular ASN may contribute to the early stages of pathogenesis in Parkinson’s disease and other synucleinopathies.Supported by a grant from The National Science Centre 2012/05/B/NZ3/02047.
14

Mitochondrial and nuclear targets of amyloid wita-evoked oxidative stress

71%
Jesko H., Strosznajder J., Cieslik M., Cakala M., Strosznajder R.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Amyloid β (Aβ) is responsible for mitochondrial failure and biochemical alterations linked to Alzheimer`s disease (AD). To better understand mechanisms of Aβ toxicity we investigated its mitochondrial and nuclear targets, apoptosis-inducing factor (AIF) and Poly(ADP-ribose) polymerase-1 (PARP-1) in PC12 cells transfected with wild type (APPwt) or double Swedish-mutated human Amyloid Precursor Protein gene (APPsw) characterized by different Aβ concentrations. We found close relationship between Aβ level and cyclooxygenase (COX)- and lipoxygenase (LOX)-related free radical formation leading to p65/NF-κB nuclear translocation. COX and LOX inhibitors protected APPsw cells against p65 translocation. Aβ-evoked oxidative stress enhanced mitochondrial AIF level and inhibited PARP-1 in APPsw cells. Nitrosative stress evoked by 0.5 mM sodium nitroprusside (SNP) had no further effect on Aβ-altered PARP-1 activity and mitochondrial AIF level in APPsw cells. However, SNP evoked death of 70–80% of all cell types after 24 h. COX and LOX inhibitors had ameliorating effect in these conditions. Our data indicated that double Swedish mutation in APP signifi cantly increased cell vulnerability to oxidative stress. Enhanced mitochondrial AIF level and PARP-1 inhibition might be responsible for cell survival under oxidative stress evoked by accumulating Aβ in APPsw cells. COX and LOX inhibitors protected the cells against death caused by simultaneous Aβ toxicity and nitrosative stress.
15

Extracellular alpha-synuclein induces calpain-dependent overactivation of cyclin-dependent kinase 5 in PC12 cells

71%
Adamczyk A., Gassowska M., Wilkaniec A., Cieslik M., Czapski G. A.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
16

Zależne od wieku zmiany biochemiczne i molekularne w mózgu młodych i starych myszy transgenicznych z APP - Tg(Thyl;APP)Va717Ile

71%
Chalimoniuk M., Gasowska M., Cieslik M., Langfort J., Kowalczyk A.
Annals of Warsaw University of Life Sciences - SGGW. Animal Science
|
2011
|
tom 48
17

Typy i właściwości gnojowicy oraz możliwości jej zagospodarowania

71%
Smurzynska A., Czekała W., Kupryaniuk K., Cieslik M., Kwiatkowska A.
Problemy Inżynierii Rolniczej
|
2016
|
tom 24
|
nr 4
18
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Wykorzystanie odpadów z przetwórstwa mięsnego na cele energetyczne

71%
Kozlowski K., Cieslik M., Smurzynska A., Lewicki A., Jas M.
Nauki Inżynierskie i Technologie
|
2015
|
nr 1(16)
Tani import oraz notowane przez ostatnie lata wysokie ceny skupu żywca są jedną z ważniejszych przyczyn nierentowności przedsiębiorstw przemysłu mięsnego. Dodatkowym problemem dla właścicieli firm z tej branży są powstające w produkcji mięsnej odpady, które powinny zostać odpowiednio zagospodarowane, co z reguły generuje wysokie koszty. Optymalnym rozwiązaniem wydaje się zastosowanie w tym celu fermentacji metanowej. Substraty, takie jak gnojowica świńska oraz treść przewodu pokarmowego, mogą być wykorzystane jako substrat dla biogazowni bez wstępnej obróbki termicznej, natomiast odpady poubojowe, w myśl Rozporządzenia Parlamentu Europejskiego i Rady (WE) nr 1069/2009 z dnia 21 października 2009 r., wymagają wcześniejszej higienizacji. W Pracowni Ekotechnologii, działającej przy Instytucie Inżynierii Biosystemów Uniwersytetu Przyrodniczego w Poznaniu, przeprowadzono badania wydajności biogazowej tych odpadów z Zakładu Mięsnego „Paszak” w Olszówce (gmina Przykona). Analizę wykonano zgodnie z obowiązującą niemiecką normą DIN 38 414/S8. Na podstawie otrzymanych wyników stwierdzono, że substraty te mają bardzo duży potencjał energetyczny. Wykazano, że racjonalne zagospodarowanie uciążliwych odpadów rzeźnych (treści przewodu pokarmowego świń i gnojowicy) może generować zysk ekonomiczny wynikający ze sprzedaży energii elektrycznej i ciepła, a także wyeliminowania kosztów związanych z utylizacją generowanych odpadów.
19

Maternal immune activation during pregnancy alters the expression of mitochondrial dynamics markers in the brain of rat offspring

71%
Zawadzka A., Cieslik M., Gewartowska M., Frontczak-Baniewicz M., Adamczyk A.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
INTRODUCTION: Prenatal exposure to infection and subsequent inflammatory responses, as well as, mitochondrial dysfunction has been implicated in the pathogenesis of autism spectrum disorders (ASDs). However, the molecular links between infection-induced fetal brain changes, mitochondrial deregulation, and the autistic phenotype remain obscure. AIM(S): Analysis of maternal immune activation (MIA)-induced changes in the expression of mitochondrial dynamics markers in the brain of the neonatal and adolescent rat offspring. METHOD(S): The MIA model was induced by single intraperitoneal injection of lipopolysaccharide (100 μg/kg b.w.) to pregnant rats at embryonic day 9.5. On the 7th or 52-53rd post-natal day, rat offspring were decapitated, and the brains isolated. Transmission electron microscopy (TEM), quantitative real‑time PCR (qPCR), and immunoblotting were used to determine mitochondrial ultrastructure and mRNA/protein expression, respectively. RESULTS: The electron microscopic study demonstrated altered mitochondrial morphology, including fragmented cristae, expanded matrix compartment, and membrane disruption in both the cerebral cortex and hippocampus of adolescent MIA offspring. Moreover, changes were noted in the expression of proteins involved in the maintenance of mitochondrial morphology. We observed upregulated fusion machinery proteins – mitofusin 1 (Mfn1), mitofusin 2 (Mfn2), and Opa1 – as well as mitochondrial fission proteins – dynamin related protein‑1 (Drp1) and fission protein 1 (Fis1) – in the neonatal MIA brains. However, in adolescent animals exposed to prenatal infection, the expression of Mfn1, Mfn2 and Opa1 was significantly reduced; nevertheless, Drp1 and Fis1 remained increased CONCLUSIONS: MIA-evoked perturbations in the proteins regulating mitochondrial dynamics reveal potentially important aspects of the mechanism linking neuroinflammation, impaired mitochondrial function, and ASD. FINANCIAL SUPPORT: Supported by the POWER Och!Doc Program and NSC grant 2016/23/D/NZ4/03572.
20
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Możliwości poprawy bilansu energetycznego i ekonomicznego biogazowni

61%
Kozlowski K., Lewicki A., Cieslik M., Janczak D., Czekala W., Smurzynska A., Brzoski M.
Technika Rolnicza Ogrodnicza Leśna
|
2017
|
nr 3
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