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N A Glushankova

Publications and source records attributed to N A Glushankova.

5 recordsLinked to original sources

[Effect of cytochalasin D on DNA synthesis in cultured cells].

The effect of cytochalasin D (CD), an agent specifically destroying actin cytoskeleton, on DNA replication of cultured mouse embryonic fibroblasts (MEF) and BALB/3T3 strain cells was studied. Incubation of normal cells with CD resulted in progressive inhibition of DNA synthesis: in the first 16-20 h the percentage of cells pulse-labelled with 3H-thymidine was similar to that in control cultures, on day 8 the percentage of labelled cells was 7-8 times lower than in the control. The transfer of cells into fresh medium upon 8-day incubation in the presence of CD resulted in the recovery of DNA synthesis. Similar curves of DNA synthesis inhibition in the presence of CD and of DNA synthesis recovery in fresh medium were observed both in mononuclear and binuclear cells. Thus, CD-induced reorganization of actin cytoskeleton can have an abrupt but reversible disturbing effect on normal cell cycle.

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[Sensitivity of the proliferation of normal and tumor cells to cytochalasin D].

The effect of cytochalasin D, which is known to disrupt specifically actin cytoskeleton, on DNA replication was studied. The incubation of cultured mouse embryonic fibroblasts (MEF), cells of Balb/3T3 line and cells of minimally transformed clones 12 MC and 6 st/T CAK-7 line with cytochalasin D leads to inhibition of DNA synthesis. A complete inhibition of labeled index in MEF culture was observed after an 8 day incubation in cytochalasin D. Part of cells of clones 12 MC and 6 st/T were insensitive to cytochalasin D and continued to enter to S-phase even after a 10 day incubation. The transfer of cells into a fresh medium leads to a rapid restoration of DNA synthesis. Strongly transformed L cells were almost insensitive to cytochalasin D. Thus, the reorganization of actin cytoskeleton caused by cytochalasin D can inhibit the cycle of normal and minimally transformed cells. In the course of neoplastic progression, in the transformed cells there is a loss of dependence of cell proliferation on microfilament system.

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Polarization of cytoplasmic fragments microsurgically detached from mouse fibroblasts.

We have studied the polarity of cytoplasm organization in tiny fragments of mouse embryo fibroblasts, produced by the microsurgical separation of long processes of cytochalasin-treated cells. In the cytochalasin-free medium fragments respread and developed small lamellas at one or both of their ends. Granules, visible at phase-contrast optics, were always collected in the central part of the fragment. Lamellas of the fragment, as well as lamellar cytoplasm of parent cells, were able to clear surface receptors patched by concanavalin A and an antibody to concanavalin A. Immunofluorescence microscopy showed that the fragments always contained actin microfilament bundles parallel to the long axis of the fragment, but microtubules were present not more than for 6 hrs after detachment of the fragments from the cell bodies. Fragments detached from the cells treated with colcemid and cytochalasin simultaneously and transferred into the drug-free medium never had any microtubules. In spite of that, their behaviour was similar to the behaviour of the fragments that were produced from the control cells treated only with cytochalasin. These results show that the small fragments of mouse embryo fibroblasts are able to maintain the polar organization of cytoplasm and the microtubules are not responsible for this organization.

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