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Results for “polyploidy”

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At least 397 records · Page 22Linked to original sources
PubMed1981

On the control of the trophoblastic giant-cell transformation in the mouse: homotypic cellular interactions and polyploidy.

Trophoblastic tissues grown under different conditions in vitro display distinct patterns of cellular growth. Thus, trophoblast cultured on 'bacteriological grade' plastic surfaces remained in suspension culture as rounded tissue fragments. Such tissues maintained numerous cell contacts and remained, in turn, largely diploid. Trophoblast explanted on a 'tissue-culture grade' substrate formed monolayers. These contained fewer cell contacts and had more giant nuclei than the rounded tissues. Finally, if trophoblast was dissociated and grown as attached single cells, so that cell contact was minimal or absent, the single-cell preparations contained more giant nuclei than tissues grown either as monolayers or in suspension. These results suggest that changes in tissue shape and the number of cell contacts can modify the growth of mouse trophoblast and alter its ability to become giant.

Animals↗
PubMed1995

The important role of PKC in controlling polyploidy formation in cultured fibrosarcoma cell line.

Induction of polyploidization by colcemid in cultured fibrosarcoma cells (Meth-A cells) was examined. Activators of protein kinase C (PKC), phorbol 12-myristate 13-acetate (PMA) and ATP, inhibited colcemid-induced polyploidization, but not colcemid-induced cell proliferation cessation. These findings suggest that a down-regulation of PKC activity results in checkpoint "dysfunction" which induces polyploidization and that inhibition of polyploidization induction by PMA and ATP is not a result of the inhibition of colcemid-induced depolymerization of tubulin.

Adenosine Triphosphate↗
PubMed1994

Mode of inheritance of the higher degree of megakaryocyte polyploidization in C3H mice. I. Evidence for a role of genomic imprinting in megakaryocyte polyploidy determination.

C3H mice have higher average ploidy megakaryocytes than all other mouse strains tested, but the mode of inheritance of this anomaly is unknown. Therefore, to clarify the genetics of high ploidy megakaryocytes in C3H mice, we measured megakaryocyte DNA content from both male and female offspring from F1, as well as backcross matings. In all, offspring from seven different matings of mice were studied: (1) C57BL X C57BL (the first strain listed is the male parent in each case), (2) B6C3F1 (offspring from C57BL X C3H mating) X C57BL, (3) C57BL X B6C3F1, (4) C57BL X C3H, (5) C3H X B6C3F1, (6) B6C3F1 X C3H, and (7) C3H X C3H. The polyploid megakaryocyte DNA content distributions of the offspring from these matings show that C3H mice have higher percentages of high ploidy megakaryocytes than did all other mice. Also, male mice had significantly higher percentages of high ploidy (32N and 64N) megakaryocytes than did female mice for all matings, except backcross mating no. 6. The megakaryocyte DNA content for individual offspring of a given backcross appeared to form a single, continuous distribution, rather than segregate into two distinct groups, suggesting that the higher megakaryocyte DNA content of C3H mice is caused by involvement of multiple allelles. This conclusion is further supported by our finding that the frequency of high ploidy megakaryocytes among offspring of the various matings was related to the proportion of C3H genotype contributed by the parents, ie, average megakaryocyte DNA content increased linearly (r2 = .88 for male mice and .84 for female mice. P < .0001) with increasing C3H gene dosage; the correlations for both male and female mice were essentially parallel (slope = 0.08 and 0.09, respectively). In addition, we found an effect of genomic imprinting on megakaryocyte DNA content in backcross offspring. The genetic imprinting was characterized by the female parent having a greater influence on the offspring's megakaryocyte DNA content than the male parent, ie, although the overall genetic makeup was the same, female offspring from backcross no. 6 (in which the female was C3H) had higher average megakaryocyte ploidy values than those from backcross no. 5 (in which the female was B6C3F1).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Development of apoptosis and polyploidy in human lymphoblast cells as a function of position in the cell cycle at the time of irradiation.

The TK6 and WI-L2-NS human lymphoblast cell lines are derived from the same donor, but WI-L2-NS cells are more resistant to killing by ionizing radiation and also contain a mutation in the coding region of the p53 gene which delays the appearance of apoptosis. To determine whether the difference in radiosensitivity is a result of the slower rate of appearance of apoptosis (referred to as the rate of apoptosis) or to other factors related to the function of p53 such as the G1-phase checkpoint, we have examined the clonogenicity and rates of apoptosis in synchronous populations of these two cell lines as a function of time after exposure to x-rays. The greater radiosensitivity of G1-phase TK6 cells compared to G1-phase WI-L2-NS cells appeared adequate to explain the difference in radiosensitivity of asynchronous cultures. However, TK6 cells irradiated in G1 phase underwent apoptosis about three times more slowly than cells irradiated in other phases of the cycle, cautioning against equating more rapid apoptosis with greater radiosensitivity. The slower rate of apoptosis of G1-phase TK6 cells could not be explained by a radiation-induced block in G1 phase since there was only a short delay in exit of cells from G1 phase. Giant cells (primarily polyploid) were formed after irradiation of WI-L2-NS but not TK6 cells, and fewer giant cells were observed 3-4 days after irradiation in WI-L2-NS cells irradiated in S phase than cells irradiated in other phases. Giant cells were lost from the population through apoptosis which occurred in a synchronous fashion in the multiple nuclei. These results highlight interesting differences in the pattern of cell death between the two cell lines and suggest that the response of TK6 cells in G1 phase, which has the slowest rate of appearance of apoptosis in spite of the fact that it is the most radiosensitive phase for clonogenic survival, may be largely responsible for the reduced shoulder on the radiation survival curve for TK6 cells compared with WI-L2-NS cells.

Apoptosis↗