Dorota Makarewicz

Mossakowski Medical Research Institute, Polish Academy of Sciences

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Jerzy W. Łazarewicz

Polish Academy of Sciences

Elżbieta Salińska

Mossakowski Medical Research Institute, Polish Academy of Sciences

Elżbieta Ziemińska

Polish Academy of Sciences

Teresa Zalewska

Polish Academy of Sciences

Małgorzata Duszczyk

ETH Zurich

Marta Słomka

Mossakowski Medical Research Institute, Polish Academy of Sciences

Apolonia Ziembowicz

Polish Academy of Sciences

Małgorzata Ziemka‐Nałęcz

Mossakowski Medical Research Institute, Polish Academy of Sciences

Wojciech Danysz

MerLion Pharma (Germany)

Małgorzata Kajta

Maj Institute of Pharmacology

Cooperative Institutions

Polish Academy of Sciences

Mossakowski Medical Research Institute, Polish Academy of Sciences

Jagiellonian University

University of Warsaw

Maj Institute of Pharmacology

Medical University of Warsaw

University of Gothenburg

Georgetown University

Institute of Pharmacology

Postgraduate School of Molecular Medicine

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Proinflammatory cytokines in injured rat brain following perinatal asphyxia.

PubMed (2002)

D. Maślińska Milena Laure‐Kamionowska A Kaliszek Dorota Makarewicz

In contrast to astrogliosis, which is common to injuries of the adult CNS, in the developing brain this process is minimal. Reasons postulated for this include the relative immaturity of the immune system and the consequent insufficient production of cytokines to evoke astrogliosis. To explore this hypothesis, the study was undertaken to detect the presence of some proinflammatory cytokines in the injured rat brain following perinatal asphyxia (ischaemia/hypoxia). The localisation of TNF-alpha, IL-15, IL-17 and IL-17 receptors was visualised by means of immunohistochemistry. In numerous neurones of the rat brain, the IL-17 appeared to be constitutively expressed. In the early period of inflammation the IL-15 was produced mainly by the blood cells penetrating the injured brain but later it was synthesised also by reactive astrocytes surrounding brain cysts and forming dense astrogliosis around necrotic brain regions. The direct effect on astrogliosis of other estimated cytokines seems to be negligible. All the results lead to the conclusion that from all cytokines identified in the injured immature rat brain the IL-15 plays the most important role during inflammatory response and participates in the gliosis of reactive astrocytes.

Astrogliosis

Proinflammatory cytokine

Gliosis

Brain damage

Perinatal asphyxia

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Citations (14)

Effects of mGluR5 positive and negative allosteric modulators on brain damage evoked by hypoxia-ischemia in neonatal rats

Folia Neuropathologica (2015)

Dorota Makarewicz Marta Słomka Wojciech Danysz Jerzy W. Łazarewicz

In the present study, we examined the effects of negative and positive allosteric modulators of metabotropic glutamate receptor 5 (mGluR5), fenobam and ADX47273, respectively, on brain damage induced by hypoxia-ischemia (H-I) in 7-day-old rats. The test drugs were administered intraperitoneally 10 min after H-I. Rectal body temperature was measured for 2.5 h after the insult. The number of apoptotic neurons in the immature rat brain was evaluated after 24 h. The wet weight of both hemispheres was determined 14 days after H-I, and its loss was used as an indicator of brain damage. In the vehicle-treated groups, H-I reduced the weight of the ipsilateral (ischemic) hemisphere by approximately 33% and sixfold increased the number of apoptotic cells in the cortex. Fenobam (10 mg/kg) and ADX47273 (5, 10, and 30 mg/kg) had no significant effect on brain damage, although application of fenobam at this dose significantly reduced the number of apoptotic cells. In contrast, fenobam (20 mg/kg) potentiated ischemic brain damage to 57.4% and had no effect on H-I-induced apoptosis. In all of the experimental groups, we detected no significant changes in the weight of the contralateral (control) hemisphere or the rectal temperature. In conclusion, in 7-day-old rats, the bidirectional modulation of mGluR5 by fenobam (10 mg/kg) and ADX47273 (all doses tested) did not result in significant changes in H-I-evoked brain damage, supporting our previous data indicating that also the antagonists of mGluR5 MPEP and MTEP, which reduce neuronal lesions in adult animals submitted to brain ischemia, were ineffective in 7-day-old rat pups.

Brain damage

Hypoxia

Allosteric modulator

10.5114/fn.2015.56544

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Neonatal cerebral hypoxia‐ischemia: involvement of FAK‐dependent pathway

International Journal of Developmental Neuroscience (2005)

Teresa Zalewska Dorota Makarewicz Bernardetta Janik Małgorzata Ziemka‐Nałęcz

Abstract Focal adhesion kinase (FAK) is a non‐receptor tyrosine kinase thought to play a major role in transducing extracellular matrix (ECM)‐derived survival signals into cells. Thus, modulation of FAK activity may affect the linkage between ECM and signaling cascade to which it is connected and may participate in a variety of pathological settings. In the present study, we investigated the effect of neonatal cerebral hypoxia‐ischemia (HI) on levels and tyrosine phosphorylation of focal adhesion kinase and the interaction of this enzyme with Src protein tyrosine kinase and adapter protein p130Cas, involved in FAK‐mediated signaling pathway. The total amount of focal adhesion kinase as well as its phosphorylated form declined substantially to about 50% of the control between 24 and 48 h after the insult. Concomitantly a decreased association of FAK with its investigated molecular partners, Src kinase and p130Cas protein has been observed. This early response to brain hypoxia‐ischemia was attenuated during prolonged recovery with almost complete return to control values at 7 days. These data are indicative of an involvement of FAK‐dependent signaling pathway in the evolution of HI‐induced neuronal degeneration.

PTK2

10.1016/j.ijdevneu.2005.05.010

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CDP-choline (citicoline) attenuates brain damage in a rat model of birth asphyxia

Acta Neurobiologiae Experimentalis (2008)

Michał Fiedorowicz Dorota Makarewicz Kinga I. Stanczak-Mrozek Paweł Grieb

To estimate protective potential of citicoline in a model of birth asphyxia, the drug was given to 7-day old rats subjected to permanent unilateral carotid artery occlusion and exposed for 65 min to a hypoxic gas mixture. Daily citicoline doses of 100 or 300 mg/kg, or vehicle, were injected intraperitoneally for 7 consecutive days beginning immediately after the end of the ischemic-hypoxic insult, and brain damage was assessed by gross zorphology score and weight deficit two weeks after the insult. Caspase-3, α-fodrin, Bcl-2, and Hsp70 levels were assessed at 0, 1, and 24 h after the end of the hypoxic insult in another group of rat pups subjected to the same insult and given a single dose of 300 mg/kg of citicoline or the vehicle. Citicoline markedly reduced caspase-3 activation and Hsp70 expression 24 h after the insult, and dose-dependently attenuated brain damage. In the context of the well-known excellent safety profile of citicoline, these data suggest that clinical evaluation of the efficacy of the drug in human birth asphyxia may be warranted.

Citicoline

Brain damage

10.55782/ane-2008-1705

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Citations (33)

NMDA receptor antagonists MK-801 and memantine induce tolerance to oxygen and glucose deprivation in primary cultures of rat cerebellar granule cells

Acta Neurobiologiae Experimentalis (2014)

Marta Słomka Magdalena Kuszczyk Jerzy W. Łazarewicz Dorota Makarewicz

Preconditioning is an experimental strategy for reducing ischemic brain damage. There are reports that brief exposure of neurons to NMDA-receptor antagonists may be an adequate preconditioning stressor. We studied effects of preconditioning of the cerebellar granule cells (CGC) in primary culture by 30-minute exposure to NMDA receptor antagonists 0.5 microM MK-801 or 5 microM memantine. CGC were challenged with oxygen and glucose deprivation (OGD) or excitotoxic glutamate and cell viability was tested 24 h later using calcein/ethidium homodimer-1 staining. We studied glutamate-induced increases in 45Ca uptake and in the intracellular Ca2+ level assessed with the fluorescent probe fluo-3. The number of living cells In OGD-treated cultures decreased by 42 percent. Preconditioning with MK-801 or memantine 24 h earlier reduced cell death to 8 percent and 30 percent and 48 h earlier to 27percent and 33 percent, respectively. Pretreatment with MK-801 followed by the standard MK-801 wash out was slightly cytoprotective in a glutamate excitotoxicity test performed immediately; the protection increased significantly 24 h after preconditioning. In both cases the extensive wash out of MK-801 after preconditioning resulted in loss of cytoprotection. The increase in the intracellular Ca2+ level evoked by glutamate was decreased 24 h after preconditioning and even halved in the neuronal cultures 48 h after preconditioning with MK-801 and memantine. Glutamate-induced 45Ca uptake in these cells was decreased by 18 percent, irrespective of the time laps after preconditioning. These results demonstrate that preconditioning of CGC with NMDA receptor antagonists induces prolonged tolerance to OGD, which is accompanied by the reduction of glutamate-evoked calcium fluxes. The causal relationship between these effects may be suggested.

Memantine

Excitotoxicity

Ischemic Preconditioning

Dizocilpine

Kainate receptor

10.55782/ane-2014-2002

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Citations (7)

The Potential Benefits of the Influenza Vaccination on COVID-19 Mortality Rate—A Retrospective Analysis of Patients in Poland

Vaccines (2021)

Kinga I. Stanczak-Mrozek Adam Sobczak Leszek Lipiński Elżbieta Sienkiewicz Dorota Makarewicz

In this study,we used publicly available data from the Centrum e-Zdrowia (CeZ) Polish Databank proposing a possible correlation between influenza vaccination and mortality due to COVID-19. We limited our search to the patients with positive COVID‑19 laboratory tests from 1 January 2020 to 31 March 2021 and who filled a prescription for any influenza vaccine during the 2019-2020 influenza season. In total, we included 116,277 patients and used a generalized linear model to analyze the data.We found out that patients aged 60+ who received an influenza vaccination have a lower probability of death caused by COVID-19 in comparison to unvaccinated, and the magnitude of this difference grows with age. For people below 60 years old, we did not observe an influence of the vaccination. Our results suggest a potential protective effect of the influenza vaccine on COVID-19 mortality of the elderly. Administration of the influenza vaccine before the influenza season would reduce the burden of increased influenza incidence, the risk of influenza and COVID‑19 coinfection and render the essential medical resources accessible to cope with another wave of COVID-19. To our knowledge, this is the first study showing a correlation between influenza vaccination and the COVID-19 mortality rate in Poland.

10.3390/vaccines10010005

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Citations (7)

Pretreatment is not mandatory for neuroprotection with 1alpha,25-dihydroxyvitamin D3 in perinatal hypoxic-ischemic rat brain damage in vivo and in excitotoxic injury of primary neuronal cell cultures

Dorota Makarewicz Małgorzata Kajta Elżbieta Ziemińska Danuta Jantas Helena Domin

Brain damage

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Hypobaric Hypoxia Postconditioning Reduces Brain Damage and Improves Antioxidative Defense in the Model of Birth Asphyxia in 7-Day-Old Rats

Neurochemical Research (2013)

Marcin Gamdzyk Dorota Makarewicz Marta Słomka Apolonia Ziembowicz Elżbieta Salińska

Hypoxia

Brain damage

Perinatal asphyxia

10.1007/s11064-013-1191-0

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Citations (20)

Original article Delayed preconditioning with NMDA receptor antagonists in a rat model of perinatal asphyxia

Folia Neuropathologica (2014)

Dorota Makarewicz Dorota Sulejczak Małgorzata Duszczyk Michał Małek Marta Słomka

AMA Makarewicz D, Sulejczak D, Duszczyk M, Małek M, Słomka M, Lazarewicz J. Original articleDelayed preconditioning with NMDA receptor antagonists in a rat model of perinatal asphyxia. Folia Neuropathologica. 2014;52(3):270-284. doi:10.5114/fn.2014.45568. APA Makarewicz, D., Sulejczak, D., Duszczyk, M., Małek, M., Słomka, M., & Lazarewicz, J. (2014). Original articleDelayed preconditioning with NMDA receptor antagonists in a rat model of perinatal asphyxia. Folia Neuropathologica, 52(3), 270-284. https://doi.org/10.5114/fn.2014.45568 Chicago Makarewicz, Dorota, Dorota Sulejczak, Małgorzata Duszczyk, Michał Małek, Marta Słomka, and Jerzy W. Lazarewicz. 2014. "Original articleDelayed preconditioning with NMDA receptor antagonists in a rat model of perinatal asphyxia". Folia Neuropathologica 52 (3): 270-284. doi:10.5114/fn.2014.45568. Harvard Makarewicz, D., Sulejczak, D., Duszczyk, M., Małek, M., Słomka, M., and Lazarewicz, J. (2014). Original articleDelayed preconditioning with NMDA receptor antagonists in a rat model of perinatal asphyxia. Folia Neuropathologica, 52(3), pp.270-284. https://doi.org/10.5114/fn.2014.45568 MLA Makarewicz, Dorota et al. "Original articleDelayed preconditioning with NMDA receptor antagonists in a rat model of perinatal asphyxia." Folia Neuropathologica, vol. 52, no. 3, 2014, pp. 270-284. doi:10.5114/fn.2014.45568. Vancouver Makarewicz D, Sulejczak D, Duszczyk M, Małek M, Słomka M, Lazarewicz J. Original articleDelayed preconditioning with NMDA receptor antagonists in a rat model of perinatal asphyxia. Folia Neuropathologica. 2014;52(3):270-284. doi:10.5114/fn.2014.45568.

Perinatal asphyxia

10.5114/fn.2014.45568

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Citations (12)

Early and delayed hypoxic postconditioning in the model of birth asphyxia in 7-day-old rats

Acta Neurobiologiae Experimentalis (2011)

Dorota Makarewicz Elżbieta Salińska

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