scholarly journals Intercellular adhesive selectivity. I. An improved assay for the measurement of embryonic chick intercellular adhesion (liver and other tissues).

1976 ◽  
Vol 68 (1) ◽  
pp. 80-89 ◽  
Author(s):  
E J McGuire ◽  
C L Burdick

An improved assay for measuring intercellular adhesive selectivity of embryonic chick liver cells is described. Three major improvements over earlier procedures are noted: (a) enhanced reproducibility of liver cell-liver cell aggregate adhesion (homotypic adhesion) was achieved; (b) 25-70% of the input cells adhered to the collecting aggregates during the course of routine experiments as compared to the 0.25% in earlier assays. This increase in cellular adhesion suggests that the observed cell pick-up is a characteristic of the majority of the dissociated liver cell population; (c) the rate of intercellular adhesion was increased 1,000-fold. The main feature of the assay is that it measures the tissue adhesive selectivities of the dissociated cell population. Studies were undertaken on three embryonic chick tissues (liver, neural retina, and mesencephalon) to determine the tissue selectivity of intercellular adhesion of these dissociated cell types. Some general properties of liver cell homotypic adhesion have been studied and are reported.

1976 ◽  
Vol 68 (1) ◽  
pp. 90-100 ◽  
Author(s):  
E J McGuire

Studies directed at understanding the molecular basis of liver cell homotypic adhesion are presented. An assay which measures the rate of adhesion of isotopically labeled (32PO4) embryonic chick liver cells to liver cell aggregates, described in a companion paper, has been used to investigate the problem of intercellular adhesive selectivity. Cation requirements, the effects of various inhibitors of metabolism and protein synthesis, of chelators (EDTA and EGTA), and the effects of temperature on liver cell adhesion are reported. Two mechanisms of inhibition of liver intercellular adhesion are suggested. One involves destruction of cell-surface adhesion receptors (sensitivity to proteases); the other is an energy-dependent step which may involve alterations in plasma membrane conformation and/or membrane fluidity. Finally, a model is suggested for liver cell-cell adhesion that incorporates the early tissue selectivity of intercellular adhesion previously reported, followed by a multistep process which leads to histogenic aggregation.


1965 ◽  
Vol s3-106 (76) ◽  
pp. 311-314
Author(s):  
W. GALBRAITH

A cheap and simple electrical counter is described which is convenient for the simultaneous assessment of the frequencies of several different characteristics in a cell population.


Author(s):  
Ioan Florin GHIURCO ◽  
Aurel DAMIAN ◽  
Vasile Florin RUS ◽  
Cristian MARTONOS ◽  
Maria Cătălina MATEI ◽  
...  

Hepatocytes represent the majority of the liver cell population and are arranged in the form of cords placed in intimate contact with the sinusoidal capillaries. The functional complexity corroborated with the intensity of the activity of hepatocytes requires large amounts of energy. The organelles involved in the production of chemical energy used in the activity of hepatocytes are the mitochondria. The purpose of this study was to verify the mitochondrial load of hepatocytes in all areas of the classical hepatic lobules, in order to indirectly assess the intensity of hepatocyte activity in each area. Materials and Methods Five fresh corpses of chinchilla (Chinchilla lanigera) from an independent breeder from Bistrița-Năsăud county were used. Liver fragments were harvested and fixated in Kolster’s solution for 24 hours, stained with Heidenhain ferric hematoxylin, and assessed using Olympus BX41 microscope. Fixation with Kolster's solution and the staining with Heidenhain's iron hematoxylin clearly shows the hepatocytic mitochondria in shades from gray to black. The liver lobules displayed an uneven distribution of mitochondria depending on the area. In zone 1 of the classical hepatic lobule, the degree of loading of hepatocytes with mitochondria is larger than in zone 2 and much larger than in zone 3. Morphological features of the hepatocytes, including the number and distribution of mitochondria in the hepatic lobules, should improve the understanding of the physiology and pathology of the liver.


Development ◽  
1980 ◽  
Vol 56 (1) ◽  
pp. 191-200
Author(s):  
Stuart A. Newman

A population of mesenchymal cells derived from the stage-25 chick wing tip gives rise to progeny of a similar morphology and to authentic fibroblasts when grown in low densityculture. Mixed clones containing both cell types are often observed. As the more rapidly proliferating fibroblasts begin to predominate in these cultures, collagen biosynthesisrises from the basal mesenchymal level to a level characteristic of mature fibroblasts. Thefibroblast progenitor is discussed relative to the other cell types of the mesodermal lineage of the developing limb.


1976 ◽  
Vol 20 (1) ◽  
pp. 29-46 ◽  
Author(s):  
H.R. Bode ◽  
K.M. Flick ◽  
G.S. Smith

Mechanisms regulating the population size of the multipotent interstitial cell (i-cell) in Hydra attenuata were investigated. Treatment of animals with 3 cycles of a regime of 24 h in 10-2 M hydroxyurea (HU) alternated with 12 h in culture medium selectively killed 95–99% of the i-cells, but had little effect on the epithelial cells. The i-cell population recovered to the normal i-cell:epithelial cell ratio of I:I within 35 days. Continuous labelling experiments with [3H]thymidine indicate that the recovery of the i-cell population is not due to a change in the length of the cell cycle of either the epithelial cells or the interstitial cells. In control animals 60% of the i-cell population undergo division daily while 40% undergo differentiation. Quantification of the cell types of HU-treated animals indicates that a greater fraction of the i-cells were dividing and fewer differentiating into nematocytes during the first 2 weeks of the recovery after HU treatment. Therefore, the mechanism for recovery involves a shift of the 60:40 division:differentiation ratio of i-cells towards a higher fraction in division until the normal population size of the i-cells is regained. This homeostatic mechanism represents one of the influences affecting i-cell differentiation.


Development ◽  
1998 ◽  
Vol 125 (6) ◽  
pp. 1059-1066 ◽  
Author(s):  
D.K. Waid ◽  
S.C. McLoon

The different retinal cell types arise during vertebrate development from a common pool of progenitor cells. The mechanisms responsible for determining the fate of individual retinal cells are, as yet, poorly understood. Ganglion cells are one of the first cell types to be produced in the developing vertebrate retina and few ganglion cells are produced late in development. It is possible that, as the retina matures, the cellular environment changes such that it is not conducive to ganglion cell determination. The present study showed that older retinal cells secrete a factor that inhibits the production of ganglion cells. This was shown by culturing younger retinal cells, the test population, adjacent to various ages of older retinal cells. Increasingly older retinal cells, up to embryonic day 9, were more effective at inhibiting production of ganglion cells in the test cell population. Ganglion cell production was restored when ganglion cells were depleted from the older cell population. This suggests that ganglion cells secrete a factor that actively prevents cells from choosing the ganglion cell fate. This factor appeared to be active in medium conditioned by older retinal cells. Analysis of the conditioned medium established that the factor was heat stable and was present in the <3 kDa and >10 kDa fractions. Previous work showed that the neurogenic protein, Notch, might also be active in blocking production of ganglion cells. The present study showed that decreasing Notch expression with an antisense oligonucleotide increased the number of ganglion cells produced in a population of young retinal cells. Ganglion cell production, however, was still inhibited in cultures using antisense oligonucleotide to Notch in medium conditioned by older retinal cells. This suggests that the factor secreted by older retinal cells inhibits ganglion cell production through a different pathway than that mediated by Notch.


2018 ◽  
Vol 52 (1) ◽  
pp. 43-63 ◽  
Author(s):  
András Szabó ◽  
Roberto Mayor

Neural crest cells are a transient embryonic cell population that migrate collectively to various locations throughout the embryo to contribute a number of cell types to several organs. After induction, the neural crest delaminates and undergoes an epithelial-to-mesenchymal transition before migrating through intricate yet characteristic paths. The neural crest exhibits a variety of migratory behaviors ranging from sheet-like mass migration in the cephalic regions to chain migration in the trunk. During their journey, neural crest cells rely on a range of signals both from their environment and within the migrating population for navigating through the embryo as a collective. Here we review these interactions and mechanisms, including chemotactic cues of neural crest cells’ migration.


2019 ◽  
Vol 11 (10) ◽  
pp. 384-393 ◽  
Author(s):  
Sarah Hyun Ji Kim ◽  
Daniel A Hammer

Abstract In order to perform critical immune functions at sites of inflammation, circulatory T lymphocytes must be able to arrest, adhere, migrate and transmigrate on the endothelial surface. This progression of steps is coordinated by cellular adhesion molecules (CAMs), chemokines, and selectins presented on the endothelium. Two important interactions are between Lymphocyte Function-associated Antigen-1 (LFA-1) and Intracellular Adhesion Molecule-1 (ICAM-1) and also between Very Late Antigen-4 (VLA-4) and Vascular Cell Adhesion Molecule-1 (VCAM-1). Recent studies have shown that T lymphocytes and other cell types can migrate upstream (against the direction) of flow through the binding of LFA-1 to ICAM-1. Since upstream migration of T cells depends on a specific adhesive pathway, we hypothesized that mechanotransduction is critical to migration, and that signals might allow T-cells to remember their direction of migration after the flow is terminated. Cells on ICAM-1 surfaces migrate against the shear flow, but the upstream migration reverts to random migration after the flow is stopped. Cells on VCAM-1 migrate with the direction of flow. However, on surfaces that combine ICAM-1 and VCAM-1, cells crawl upstream at a shear rate of 800 s−1 and continue migrating in the upstream direction for at least 30 minutes after the flow is terminated—we call this ‘migrational memory’. Post-flow upstream migration on VCAM-1/ICAM-1 surfaces is reversed upon the inhibition of PI3K, but conserved with cdc42 and Arp2/3 inhibitors. Using an antibody against VLA-4, we can block migrational memory on VCAM-1/ICAM-1 surfaces. Using a soluble ligand for VLA-4 (sVCAM-1), we can promote migrational memory on ICAM-1 surfaces. These results indicate that, while upstream migration under flow requires LFA-1 binding to immobilized ICAM-1, signaling from VLA-4 and PI3K activity is required for the migrational memory of CD4+ T cells. These results indicate that crosstalk between integrins potentiates the signal of upstream migration.


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