Search

It is known that mitochondrial dysfunction can be a trigger or a concomitant mechanism in the development of Alzheimer's disease. It is also known that the restoration of intracellular mitochondrial activity of neurons and cerebral endotheliocytes is possible due to the transfer of intact mitochondria from other brain cells—in particular, astrocytes—and this transfer of mitochondria is mediated by the CD38 protein and functionally linked to it connexin 43 (Cx43). It follows that these molecules are promising for study both in relation to the mechanisms of development of neurodegeneration and in relation to the possible modulation of their activity for the correction of neurological deficits. The aim of this work was to study changes in the number of CD38- and Cx43-immunopositive cells in the neurovascular unit and the blood–brain barrier (BBB) of the brain in experimental Alzheimer's disease. We have shown that the toxic effect of β-amyloid leads to a significant increase in the number of CD38- and Cx43-positive cells as in the hippocampus of animals in vivo, and as part of the BBB model in vitro. We have also shown that the cultivation of isolated astrocytes in the presence of β-amyloid leads to an increase in the content of Cx43 in cells and that the permeability of these half-channels significantly increases. [ABSTRACT FROM AUTHOR]

Using differential G-staining of chromosomes, the karyotype of the endothelial cell line ECV304 obtained from endotheliocytes of the human umbilical vein was studied. The cells have been shown to have a polyploid karyotype with a number of chromosomes ranging from 96 to 112, as well as multiple numerical and structural clonal chromosome abnormalities. The structural rearrangements involve almost all chromosomes of the karyotype. Several paired chromosomal rearrangements have been revealed and include del(9)(p21), as well as two derivates of chromosome 3 with a breakpoint at the p25 locus, i.e., der(3)t(3;12)(3p25;12q11∼12;12q21∼24.?1) and der(3)t(3;?)(3p25). The role of these rearrangements in the immortalization of endotheliocytes and in angiogenesis is discussed. A comparison of the karyotypes of the cell line ECV304 and of the bladder carcinoma T24 cell line has shown that these karyotypes differ in all of the main cytogenetic characteristics. No identical structural chromosomal rearrangements, nor rearrangements characteristic of bladder carcinoma cells have been revealed. The studied endothelial cell line ECV304 is not identical to the T24 cell line. [ABSTRACT FROM AUTHOR]