Abstract
Oxidative stress (OS) is the condition that occurs when the anti-oxidative capacity of tissues and cells is overcome. The oxidative damage of cells is caused by free radicals which are products of OS. Lipid peroxidation is an autocatalitic process caused by OS which damages lipids and causes production of highly reactive species such as 4-hyroxynonenal (HNE). Recent findings have shown an increase in HNE-immunopositivity when compared to grade of astrocytic tumors. The cancer stem cell hypothesis suggests that not all cells in the tumor have the same ability to proliferate and maintain the growth of the tumor. Only a relatively small fraction of cells in the tumor, termed cancer stem cells, posses the ability to proliferate and self-renew extensively and expresses the surface marker CD133 (prominin-1). CNS tissue damage via trauma, viruses and ishaemia, increases the amount of OS production, which damages endothelial cells and consequently results in excess production of bone marrow-derived endothelial progenitor cells (EPCs). EPCs are immunoreactive for CD133 and CD34 and are thus important in the process of angiogenesis. Results of our study confirmed the main hypothesis, i.e.the proportional expression and distribution of CD133 and HNE in tumor cells, mesenchymal stroma, blood vessels and in the areas of necrosis, probably due to permanent OS in tumors, whose products continue to damage the endothelial cells and cause an excess production of EPCs. Identification of coexpression HNE and CD133 in GBM has important implication for the understanding of propagation of tumors into higher grade.
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Kolenc, D., Jakovčević, A., Macan, M. et al. The co-expression of 4-hydroxynonenal and prominin-1 in glioblastomas. Translat.Neurosci. 2, 163–167 (2011). https://doi.org/10.2478/s13380-011-0012-7
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DOI: https://doi.org/10.2478/s13380-011-0012-7