Browsing by Author "Schaade, L."

In the membrane of mouse macrophages two gangliosides were detected which inhibit the division of murine mastocytoma P815 turner cells. The two gangliosides were incorporated into the cytoplasmatic membrane of mastocytoma cells. The concentration necessary to achieve a complete inhibition of P815 tumor cell division is about 1 muM for both effective gangliosides. Macrophage ganglioside-induced inhibition of cell division is accompanied by morphological changes of the mastocytoma cells. While the cells art: rounding, their diameter increases and serotonin and granules appear in the cytoplasm of the enlarged cells. Our findings suggest that macrophage gangliosides may differentiate mastocytoma cells into mast cells.

Stimulation of Epstein-Barr virus (EBV) genome-positive Burkitt lymphoma cells with the ganglioside IV(3)NeuAc-nLcOse(4)Cer leads to the induction of cell differentiation processes and activates the EBV lytic viral cycle. In cells of the Burkitt lymphoma line Raji differential expression of host cell genes was analysed in the early phase (150 min) post stimulation with the ganglioside to display the cell activities that precede the activation of the EBV lytic cycle using the differential display reverse transcription-polymerase chain reaction technique. Multiple fragment cDNAs derived from control cells and ganglioside-stimulated cells were amplified using random primers and displayed via polyacrylamide gel electrophoresis. The expression pattern of 8,400 bands was analysed. Eleven differentially expressed fragment cDNAs were reamplified and identified by nucleotide sequencing. Six of these could be identified as coding for proteins that may take part in virus reactivation and differentiation. The most striking finding was the induction of s-adenosylhomocysteine hydrolase (AHCY) expression. The cellular enzyme AHCY plays an important role in transmethylation reactions controlling the replication of several viruses. Thus, an involvement in EBV replication can be suggested.