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1

Axonal outgrowth stimulation after alginate/mesenchymal stem cell therapy in injured rat spinal cord

100%
Blasko J., Szekiova E., Slovinska L., Kafka J., Cizkova D.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr 4
Despite strong efforts in the field, spinal cord trauma still belongs among the untreatable neurological conditions at present. Given the complexity of the nervous system, an effective therapy leading to complete recovery has still not been found. One of the potential tools for supporting tissue regeneration may be found in mesenchymal stem cells, which possess anti‑inflammatory and trophic factor‑producing properties. In the context of transplantations, application of degradable biomaterials which could form a supportive environment and scaffold to bridge the lesion area represents another attractive strategy. In the present study, through a combination of these two approaches we applied both alginate hydrogel biomaterial alone or allogenic transplants of MSCs isolated from bone marrow seeded in alginate biomaterial into injured rat spinal cord at three weeks after spinal cord compression performed at Th8‑9 level. Following three‑week survival, using immunohistochemistry we studied axonal growth (GAP‑43 expression) and both microglia (Iba‑1) and astrocyte (GFAP) reactions at the lesion site and in the segments below and above the lesion. To detect functional improvement, during whole survival period we performed behavioral analyses of locomotor abilities using a classical open field test (BBB score) and a Catwalk automated gait analyzing device (Noldus). We found that despite the absence of locomotor improvement, application of both alginate and MSCs caused significant increase in the number of GAP‑43 positive axons.
2

Hypothermia in the course of acute traumatic spinal cord injury

86%
Kafka J., Lukacova N., Sulla I., Maloveska M., Vikartovska Z., Cizkova D.
Acta Neurobiologiae Experimentalis
|
2020
|
tom 80
|
nr 2
In this review we briefly discuss animal experiments involving acute traumatic spinal cord injury (SCI) and the need for larger animals in testing experimental therapies. This literature overview, including the discussion of our own results from animal models, examines the use of hypothermia as a treatment method for SCI. Finally, we report the results of hypothermia application in clinical trials. Minipigs have been proposed as a potentially preferable model to rodents (typically rats) for predicting outcomes in human SCI due to their closer anatomical similarity to humans. In various animal studies, hypothermic treatment applied in the acute phase after SCI has resulted in neuroprotective effects, most likely due to inhibition of blood flow and oxygen consumption and reduction of overall metabolic activity and inflammation, resulting in improved nerve tissue sparing. Small‑scale human clinical trials have been carried out, involving general (whole‑body, systemic) or local hypothermia (close to the SCI site), with encouraging results. Nevertheless, further multi‑center, randomized, double‑blind studies with much larger patient numbers are necessary so that protocols can be standardized in order for hypothermia treatment to be reliably applied in clinical practice.
3

Comparison of dynamic behavior and maturation of neural multipotent cells derived from different spinal cord developmental stages: an in vitro study

86%
Slovinska L., Szekiova E., Blasko J., Devaux S., Salzet M., Cizkova D.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr 1
Neural progenitor cells (NPCs) are characterized as undifferentiated cells with the ability of self-renewal and multipotency to give rise to other cells of the nervous system. In our in vitro study we demonstrate the proliferative and differentiative potential of NPCs isolated from the spinal cord at different developmental stages (embryonal, early postnatal, adult), maintained and expanded within neurospheres (NSs). Using the NSs culture system, we examined the size, number of NSs and their fate when exposed to differentiation conditions. Based on immunocytochemical analyses for cell markers (MAP 2, GFAP, RIP) we evaluated the occurrence of various cell types: neurons, astrocytes and oligodendrocytes. The results show that NSs increased in size during cultivation time via NPC proliferation, but proliferation potential decreased during maturation stages. In addition, NPCs derived from spinal cord developmentally different stages gave rise to a consistent ratio of glial and neuronal progeny (3:1), and adult tissues represent a comparable source of NPCs compared to embryonal and early postnatal tissues. These data provide useful information for large-scale in vitro expansion of NPCs required for potential cell therapy after spinal cord injury.
4

Transien brain ischemia affects blood level of brain-derived neurotropic factor in early reperfusion

86%
Kravcukowa P., Danielisova V., Nemethova M., Burda J., Cizkova D., Gottlieb M.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Brain-derived neurotrophic factor (BDNF) acts on certain neurons of the central and peripheral nervous system, helps to support the survival, encourage the growth and differentiation of new neurons and synapses. In our study we monitored BDNF blood level in course of brain ischemia-reperfusion in rat models of transient focal (FI) and global (GI) ischemia. Blood samples were collected before and during ischemia and at 40 and 90 min of reperfusion. Results showed that in model of FI BDNF concentration in total blood, in plasma and blood cells rapidly decreased during fi rst 40 min of ischemia. In samples of whole blood and blood cells BDNF started to rise at the end of ischemic insult to control level, but in plasma it signifi cantly decreased. In model of GI we didn’t observe important changes after insult. During fi rst 90 min of reperfusion in both models BDNF level in total blood and in blood cells continuously decreased. Plasma level of BDNF started to rise at 40 min of reperfusion. At 90 min of recirculation BDNF level in model of FI reached 92%, in GI about 155%. In conclusion we can state that brain ischemia causes reduction of BDNF level during ischemia and subsequent elevation of BDNF concentration in blood cells at the end of ischemic insult followed by decreasing in early period of reperfusion. On the other side, plasma level of this protein reduced during ischemia markedly rises during recirculation. Supported by VEGA 2/0141/09, VEGA 2/0146/09, APVV LPP023506, APVV-51-002105.
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