The aim was to study the role of major histocompatibility complex (MHC), in mice named H-2, during early allogeneic reactions (AR) of brain cortex cells or lymphocytes. We used neuronal and glial enriched perikarya, spleen and thymus lymphocytes or their subpopulations. Rat AR was also assayed between C-6 astrocytoma cells and spleen lymphocytes. We demonstrated that: 1) H-2 dependent stimulation of Na+,K+-ATPase and ouabain- sensitive K+-dependent p-nitrophenylphosphatase (K+-pNPPase) activities represented specific response in both AR of unseparated brain cells or lymphocytes. On the other hand, non-specific AR-induced stimulation of Ca2 + - ATPase activity was observed. 2) Allogeneic enriched glial fractions reacted similarly by the same enzyme activation in contrast to no change in AR between enriched neuronal fractions. Allorecognition ability of glial cells was confirmed by AR between C-6 astrocytoma cells and lymphocytes. 3) Mature thymus lymphocytes exerted alloreactivity by specific activation of Na+,K+-ATPase or K+-pNPPase, in contrast to no change in AR between immature lymphocyte subpopulations. 4) MHC Class II monoclonal antibody inhibited Na+,K+-ATPase and K+-pNPPase activities in brain cells as well as in thymus and spleen lymphocytes in a dose-dependent manner. Results support former studies about alloantigen-induced uncoupling in brain oxidative cortex metabolism (Kovářů Med. Biol. 58: 273, 1980) via Na+,K+-ATPase and K+-pNPPase inhibition by mechanism which can mimic MHC restriction.
The fads2 gene encoding Δ6-desaturase, the rate-limiting enzyme of the LCPUFA biosynthesis is expressed in astrocytes. Dietary fatty acids, which cross the blood-brain barrier, may regulate the transcription of lipogenic enzymes through activation of transcription factors such as peroxisome proliferator-activated receptors (PPARs). The PPARs form the transcription complex with retinoid X receptors (RXRs) that are activated by 9-cis retinoic acid, a metabolite of vitamin A (VA). The study examines whether challenge of astrocytes with VA, prior 24-h treatment with palmitic acid (PA), α-linolenic acid (ALA) or docosahexaenoic acid (DHA) has the effect on the FADS2 expression. RT-qPCR showed that in astrocytes not challenged with VA, PA increased fads2 gene expression and DHA decreased it. However, in VA-primed astrocytes, PA doubled the FADS2 mRNA levels, while DHA increased fads2 gene expression, oppositely to non-primed cells. Furthermore, similar changes were seen in VA-primed astrocytes with regard to Δ6-desaturase protein levels following PA and DHA treatment. ALA did not have any effect on the FADS2 mRNA and protein levels in either VA-primed or non-primed astrocytes. These findings indicate that in the presence of vitamin A, DHA upregulates fads2 gene expression in astrocytes., B. Dziedzic, D. Bewicz-Binkowska, E. Zgorzynska, D. Stulczewski, L. Wieteska, B. Kaza, A.Walczewska., and Obsahuje bibliografii
Estrogen replacement therapy could play a role in the reduction of injury associated with cerebral ischemia in vivo, which could be, at least partially, a consequence of estrogen influence of glutamate buffering by astrocytes during hypoxia/ischemia. Estrogen exerts biological effects through interaction with its two receptors: estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ), which are both expressed in astrocytes. This study explored effects of hypoxia and glucose deprivation (HGD), alone or followed by 1 h recovery, on ERα and ERβ expression in primary rat astrocyte cultures following 1 h exposure to: a) 5 % CO2 in air (control group-CG); b) 2 % O2/5 % CO2 in N2 with glucose deprivation (HGD group-HGDG); or c) the HGDG protocol followed by 1 h CG protocol (recovery group-RG). ER α mRNA expression decreased in HGDG. At the protein level, full-length ER α (67 kDa) and three ER α -immunoreactive protein bands (63, 60 and 52 kDa) were detected. A significant decrease in the 52 kDa band was seen in HGDG, wh ile a significant decrease in expression of the full length ERα was seen in the RG. ERβ mRNA and protein expression (a 54 kDa single band) did not change. The observed decrease in ER α protein may limit estrogen-mediated signalling in astrocytes during hypoxia and recovery., M. D. Al-Bader, S. A. Malatiali, Z. B. Redzic., and Obsahuje bibliografii a bibliografické odkazy
The effect of L-glutamate, kainate and N-methyl-D-aspartate (NMDA) on membrane currents of astrocytes, oligodendrocytes and their respective precursors was studied in acute spinal cord slices of rats between the ages of postnatal days 5 and 13 using the whole-cell patch-clamp technique. L-glutamate (10~3 M), kainate (10-3 M), and NMDA (2xl0-3 M) evoked inward currents in all glial cells. Kainate evoked larger currents in precursors than in astrocytes and oligodendrocytes, while NMDA induced larger currents in astrocytes and oligodendrocytes than in precursors. Kainate-evoked currents were blocked by the AMPA/kainate receptor antagonist CNQX (10-4 M) and were, with the exception of the precursors, larger in dorsal than in ventral horns, as were NMDA-evoked currents. Currents evoked by NMDA were unaffected by CNQX and, in contrast to those seen in neurones, were not sensitive to Mg2 + . In addition, they significantly decreased during development and were present when synaptic transmission was blocked in a Ca2+-free solution. NMDA-evoked currents were not abolished during the block of K+ inward currents in glial cells by Ba2+; thus they are unlikely to be mediated by an increase in extracellular K+ during neuronal activity. We provide evidence that spinal cord glial cells are sensitive to the application of L-glutamate, kainate and transiently, during postnatal development, to NMDA.