scholarly journals Cell proliferation and cell density of mesenchyme in the maxillary process and adjacent regions during facial development in the chick embryo

Development ◽  
1978 ◽  
Vol 46 (1) ◽  
pp. 65-74
Author(s):  
Robert Minkoff ◽  
Amy J. Kuntz

Cell proliferation, as measured by DNA labeling indices was analyzed during the early development of the maxillary process. Chick embryos were labeled with [3H]thymidine for .1 h and processed for autoradiography. The percentage of labeled mesenchymal cells was determined within delineated areas in the maxillary processes and in adjacent regions. Analysis of labeling indices in each of the areas at successive stages of development demonstrated a pattern of declining rates of cell proliferation with advancing developmental age. Cell proliferation in adjacent regions declined earlier and, in some instances, faster than it did in the maxillary process. Cell density was measured in the maxillary process and the roof of the stomodeum and was found to be higher in the maxillary process throughout the period studied. Cell density and cell proliferation data were analyzed with reference to the operation of ‘density-dependent inhibition’ of growth as a regulatory mechanism for the observed changes. ‘Density-dependent inhibition’ of growth was not a satisfactory explanation for the observed differences between the maxillary process and adjacent regions.

2021 ◽  
Author(s):  
Trina Roy ◽  
Sinchan Ghosh ◽  
Bapi Saha ◽  
Sabyasachi Bhattacharya

Abstract Cell proliferation often experiences a density-dependent intrinsic proliferation rate (IPR) and negative feedback from growth-inhibiting molecules in culture media. The lack of flexible models with explanatory parameters fails to capture such a proliferation mechanism. We propose an extended logistic growth law with the density-dependent IPR and additional negative feedback. The extended parameters of the proposed model can be interpreted as density-dependent cell-cell cooperation and negative feedback on cell proliferation. Moreover, we incorporate further density regulation for flexibility in the model through environmental resistance on cells. The proposed growth law has similarities with the strong Allee model and harvesting phenomenon. We also develop the stochastic analog of the deterministic model by representing possible heterogeneity in growth-inhibiting molecules and environmental perturbation of the culture setup as correlated multiplicative and additive noises. The model provides a maximum sustainable stable cell density (MSSCD) and a new fitness measure for proliferative cells. The proposed model shows superiority to the logistic law after fitting to real cell culture datasets. We illustrate both MSSCD and the new cell fitness for a range of parameters. The cell density distributions reveal the chance of overproliferation, underproliferation, or decay for different parameter sets under the deterministic and stochastic setups.


Development ◽  
1977 ◽  
Vol 40 (1) ◽  
pp. 1-21
Author(s):  
Dennis Summerbell

Removal of the apical ectodermal ridge causes a reduction in the rate of outgrowth of the wing-bud and the loss of distal parts. More specifically it causes a short-term increase in cell density and cell death and a decrease in the rate of cell proliferation. The evidence supports the hypothesis of density-dependent control of cell division and suggests that there may also be a mechanism regulating skeletal length at the time of differentiation. An informal model is presented to explain the observations.


1974 ◽  
Vol 16 (1) ◽  
pp. 181-188
Author(s):  
MARGARET M. YARNELL ◽  
H. P. SCHNEBLI

3T3 mouse fibroblasts are released from density-dependent inhibition of growth by treatment with insulin. The same insulin treatment stimulates cell locomotion several hours before any new mitoses become visible. Inhibition of cell locomotion by colcemid does not affect the overgrowth stimulation due to insulin. From this it is concluded that cellular locomotion is not a prerequisite for the release from density-dependent inhibition of growth.


Development ◽  
1980 ◽  
Vol 57 (1) ◽  
pp. 37-49
Author(s):  
Robert Minkoff

Variation in rates of cell proliferation along the long axis of the maxillary process, within the lateral nasal process and in the zone of attachment between these structures was analyzed employing DNA labeling indices. Chick embryos were labeled with [3H]thymidine for 1 h and processed for histology and autoradiography. The percentage of labeled mesenchymal cellswas determined in delineated areas. Analysis of labeling indices indicated that rates of cell proliferation varied withineach of the facial processes. Regions where rates of proliferation were maintained at elevated levels were the boundary areas of the facial processes (e.g. the anterior tip of the maxillary process) and the zones of attachment between the facial processes (e.g. between the maxillary process and the lateral nasal process). Despite the presence of elevated rates of proliferation in selected regions within the facial processes, however, the percentage of labeled cells in all areas declined with advancing developmental age. These findings support the hypothesis, proposed by Streeter and Patten, that the ‘merging’ of adjacent facial primordia, such as the maxillary and lateral nasal processes, is accomplished by elevated rates of cell proliferation within the zones of attachment compared to the rates of proliferation in adjacent regions.


1977 ◽  
Vol 25 (1) ◽  
pp. 73-86
Author(s):  
D.S. Straus ◽  
J. Jonasson ◽  
H. Harris

We have studied the growth in vitro of a lymphoma × fibroblast hybrid and several melanoma × fibroblast hybrids in which malignancy is suppressed. The parental cells, the hybrids, and malignant segregants derived from the hybrids were analysed for serum requirement, cloning efficiency in soft agarose, density-dependent inhibition of growth, and secretion of plasminogen-activating enzyme. One malignant segregant from the lymphoma × fibroblast cross was found by a number of criteria to have a more highly ‘transformed’ phenotype than the hybrid from which it was derived. However, in the case of the melanoma × fibroblast crosses, none of the parameters examined could be correlated in a direct way with malignancy.


1983 ◽  
Vol 97 (1) ◽  
pp. 276-279 ◽  
Author(s):  
S W Peterson ◽  
V Lerch

3T3 plasma membranes were added to subconfluent cultures of SV3T3 cells in the presence of fusogens. If this protocol results in the introduction into the SV3T3 cell membrane of 3T3 plasma membrane components responsible for density-dependent inhibition of growth, then the SV3T3 cell cultures would be expected to show decreased rates of DNA synthesis as they approach confluence. Results of these experiments indicate that rates of DNA synthesis in SV3T3 cultures so treated were as much as 63% less than in untreated controls. This effect could not be attributed to the fusogens or to the 3T3 plasma membranes alone. This growth-inhibitory effect is specific for 3T3 membranes and is not observed when SV3T3 plasma membranes are fused with SV3T3 cell cultures. These data support the hypothesis that one aspect of the loss of density-dependent inhibition of growth in SV3T3 cells is a deletion or alteration in plasma membrane components and, further, that density-dependent inhibition of growth can be in part restored to SV3T3 cell cultures by fusing the cells with 3T3 plasma membranes.


1980 ◽  
Vol 85 (2) ◽  
pp. 377-385 ◽  
Author(s):  
A Vogel ◽  
R Ross ◽  
E Raines

The effects of platelet-derived growth factor and plasma components on saturation density in cultures of 3T3 cells were investigated. Both of these components of whole blood serum affect saturation density; however, when 3T3 cells become quiescent at high density in medium containing whole blood serum, only platelet-derived growth factor and fresh whole blood serum are capable of stimulating proliferation. Addition of fresh plasma- derived serum has little effect on cell growth. These results suggest that the platelet factor is the major determinant of saturation density in cultures of 3T3 cells maintained in medium supplemented with whole blood serum. Experiments were performed to investigate the mechanism by which platelet-derived growth factor regulates saturation density. We investigated the possibilities of inactivation of growth factors by proliferating cells, and the effects of cell density on the response of 3T3 cells to platelet-derived growth factor. The amount of platelet- derived growth factor required to initiated DNA synthesis increases with increasing cell density. Some inactivation of growth factors by growing cells was detected, but this depletion was only evident at high cell density. We propose that density-dependent inhibition in cultured 3T3 cells is the result both of an increased requirement for the platelet- derived growth factor as the cultures become more crowded and of inactivation of growth factor activity by growing cells.


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