THE FEATURES OF CONNEXINS EXPRESSION IN THE CELLS OF NEUROVASCLAR UNIT IN NORMAL CONDITIONS AND HYPOXIA IN VITRO
https://doi.org/10.20538/1682-0363-2014-6-5-9
Abstract
The aim of this research was to assess a role of connexin 43 (Cx43) and associated molecule CD38 in the regulation of cell-cell interactions in the neurovascular unit (NVU) in vitro in physiological conditions and in hypoxia.
Materials and methods. The study was done using the original neurovascular unit model in vitro. The NVU consisted of three cell types: neurons, astrocytes, and cerebral endothelial cells derived from rats. Hypoxia was induced by incubating cells with sodium iodoacetate for 30 min at37 °C in standard culture conditions.
Results. We investigated the role of connexin 43 in the regulation of cell interactions within the NVU in normal and hypoxic injury in vitro. We found that astrocytes were characterized by high levels of expression of Cx43 and low level of CD38 expression, neurons demonstrated high levels of CD38 and low levels of Cx43. In hypoxic conditions, the expression of Cx43 and CD38 in astrocytes markedly increased while CD38 expression in neurons decreased, however no changes were found in endothelial cells. Suppression of Cx43 activity resulted in down-regulation of CD38 in NVU cells, both in physiological conditions and at chemical hypoxia.
Conclusion. Thus, the Cx-regulated intercellular NAD+-dependent communication and secretory phenotype of astroglial cells that are the part of the blood-brain barrier is markedly changed in hypoxia.About the Authors
A. V. MorgunRussian Federation
N. V. Kuvacheva
Russian Federation
Ye. D. Khilazheva
Russian Federation
T. Ye. Taranushenko
Russian Federation
A. B. Salmina
Russian Federation
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Review
For citations:
Morgun A.V., Kuvacheva N.V., Khilazheva Ye.D., Taranushenko T.Ye., Salmina A.B. THE FEATURES OF CONNEXINS EXPRESSION IN THE CELLS OF NEUROVASCLAR UNIT IN NORMAL CONDITIONS AND HYPOXIA IN VITRO. Bulletin of Siberian Medicine. 2014;13(6):5-9. (In Russ.) https://doi.org/10.20538/1682-0363-2014-6-5-9