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1

Produkcja i wykorzystanie biogazu w oczyszczalniach ścieków w województwie śląskim

100%
Krzemien J.
Ochrona Środowiska i Zasobów Naturalnych
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2012
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nr 54
2

High-throughput assays for measuring oxidative stress and mitochondrial dysfunction in neuronal cell cultures

63%
Krzemien J., Jacobsson S.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
Drugs of abuse may cause acute as well as chronic damage to the nervous system, and a common mechanism of neurotoxicity is to induce disturbances in mitochondrial function. The mitochondrion is also an important source for cytotoxic reactive oxygen species (ROS). If the mitochondrial membrane potential (MMP) becomes depolarized, it can increase the production of ROS. This project has evaluated whether the fluorophore JC-1, which measures the depolarization of MMP, and the fluorophore H2DCFDA that oxidizes and produce fluorescence in the presence of oxygen radicals, are useful tools to screen for drug-induced neurotoxicity. The studies have been performed in embryonal carcinoma (EC) P19 cells that are pluripotent and upon retinoic acid (RA)-treatment will differentiate in culture into neurons, astrocytes and oligodendrocytes. In order to determine the predictive validity of the model/methods, a number of compounds known to cause oxidative stress and mitochondrial dysfunction have been examined (hydrogen peroxide, ionomycin, sodium azide). Main techniques employed culturing, induction and differentiation of neuronal cells, pharmacological dose-response experiments, detection and quantification of fluorescence using microplate reader and fluorescence microscopy, microplate-based colorimetric methods for assessment of cell viability, pharmacological/toxicological data and statistical analyses using the GraphPad prism software.
3

Amotl1: a novel synaptic protein important for mice social behavior and brain organization

39%
Krzemien J., Rojek K., Winiarski M., Boguszewski P. M., Knapska E., Proszynski T. J.
Acta Neurobiologiae Experimentalis
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2019
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tom 79
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nr Suppl.1
INTRODUCTION: The angiomotin family comprises of three scaffold proteins – Amot, Amotl1, and Amotl2 – that have been implicated in the regulation of cell polarity, migration, and proliferation. Recent in vitro studies have reported that Amot localizes to the synapses in mature neurons and regulates dendritic spine maturation. AIM(S): We have found that Amot, together with Yap1, the Hippo pathway transcription co‑activator, are critical for proper dendritic arborization and mice locomotor coordination. However, to date the function of the two other Angiomotins, Amotl1 and Amotl2, in neurons has not been investigated. METHOD(S): To study Amotl1 function in the mouse brain, we generated systemic and neuron-specific knock‑out (KO) mice. To assess general locomotion, we performed an open field test. Amotl1 KO mice sociability was evaluated with the three-chamber task, automatic Eco‑Hab approach, and nesting test. To record the animal’s anxiety response, we used the marble burying test. RESULTS: In the present study, we show that Amotl1 localizes to the synaptic compartments in neurons. Deletion of Amotl1 leads to hyperlocomotion, decreased anxiety-like behavior, and alteration in mice sociability. Amotl1 ablation causes an increase in volume of lateral ventricles in the mouse brain by 50%. These features have been previously observed in animal models of various psychiatric disorders, such as schizophrenia or autism. Interestingly, mass spectrometry analysis of neuron‑specific interactors demonstrated that Amotl1 binds to FMR1 and FXR1, mutations of which cause Fragile X syndrome. CONCLUSIONS: We identified a novel synaptic protein, Amotl1, the deletion of which causes behavioral deficits and that it could be a potential molecular target for the development of new therapeutics for neurological disorders. FINANCIAL SUPPORT: This research was supported by National Science Center (NCN) grants: UMO- ‑2018/29/B/NZ3/02675, UMO-2018/29/N/NZ3/02682.
4

The role of Amot and Yap1 in the regulation of dendritic tree morphogenesis and cerebellar functions

39%
Rojek K., Krzemien J., Dolezyczek H., Rylski M., Kaczmarek L., Jaworski J., Proszynski T. J.
Acta Neurobiologiae Experimentalis
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2019
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tom 79
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nr Suppl.1
INTRODUCTION: The Amot‑Yap1 complex plays a major role in the regulation of cell contact inhibition, cellular polarity and growth in many cell types. However, the function of the Amot and Hippo pathway transcription co‑activator Yap1 in the CNS remains unclear. Recent studies have demonstrated that, in mature hippocampal neurons, Amot localizes to dendritic spines where it associates with synaptic protein and regulates actin cytoskeleton. However, its function during neuronal development has not been studied. METHOD(S): Cultured primary neurons were used for RNAi experiments. For in vivo functional analysis, we used Amot and Yap1 conditional KO mice. For deletion in single sparse neurons, mice were injected with low doses of AAV‑CRE. For behavioral analysis, we used rotarod, catwalk, and foot fault tests. RESULTS: We demonstrate that Amot is a critical mediator of dendritogenesis in cultured hippocampal cells and Purkinje cells in the brain. Amot function in developing neurons depends on interactions with Yap1, which is also indispensable for dendrite growth and arborization in vitro. Conditional deletion of Amot or Yap1 in neurons leads to decreased Purkinje cell dendritic tree complexity, abnormal cerebellar morphology, and impaired motor coordination. The ability of Amot and Yap1 to regulate dendritic growth depends on regulation of S6 kinase activity and phosphorylation of S6 ribosomal protein. Hence, we suggest that Amot and Yap1 control dendritic tree morphogenesis through a cross‑talk with the PI3K/mTOR pathway, a known regulator of dendritogenesis. CONCLUSIONS: We identify a novel role for the scaffold protein Amot and the Hippo pathway transcription co‑activator Yap1 in dendritic morphogenesis. FINANCIAL SUPPORT: This research was supported by National Science Center grants 2012/05/E/ NZ3/00487 and 2015/19/N/NZ3/02346.
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