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PubMed1985

Concurrent disappearance of N-acylethanolamine glycerophospholipids and phagolysosomes enriched in N-acylethanolamine glycerophospholipids as Dictyostelium discoideum cells aggregate.

As the cellular slime mold, Dictyostelium discoideum, undergoes development, a phospholipid fraction containing 80% N-acylethanolamine glycerophospholipids (NAEGPs) and 20% acylphosphatidylglycerol (APG) disappears during the aggregation stage. In this study, the subcellular distribution of that NAEGP phospholipid fraction and the precise time period of disappearance of the fraction were determined. The content of the NAEGP fraction was determined in aggregating cells at 2-h intervals from the beginning of the developmental phase through 14 h, when the cells were completely aggregated. The NAEGP fraction comprised about 8% of the phospholipids in amoebae just starting the development cycle and about 12% in cells between 2 and 6 h of development; then its level decreased until it could not be detected at 12 and 14 h of development. The mole percentage of the total lipid phosphate in the NAEGP fraction was determined in isolated subcellular organelles. The phagolysosomes were enriched in the NAEGP fraction 1.7-2-fold over the level found in the amoebae and about 8-fold over the level in fractions highly enriched in the plasma membrane, mitochondria or peroxisomes. The content of phagolysosomes was determined by electron microscopy of aggregating cells. The amoebae contained large amounts of phagolysosomes up to 6 h of development, and then they gradually disappeared between 6 and 12 h of development. This combination of quantitative phospholipid analysis, subcellular organelle isolation and electron microscopy has revealed that in D. discoideum amoebae, the phagolysosomes were selectively enriched in the NAEGP fraction and both the NAEGP-enriched phagolysosomes and the NAEGPs disappeared concurrently between 6 and 12 h of development.

Dictyostelium↗
PubMed1997

Analysis of factors contributing to the formation of mononuclear cell aggregates ("escapees") in flow cytometric immunophenotyping.

During immunostaining, human lymphocytes may form aggregates with activated platelets and monocytes, resulting in increased forward (FSC) and sideward (SSC) light scatter signals. Consequently, aggregated cells "escape" from the standard FSC-SSC analysis gate, thereby producing erroneous results. We observed that the frequency of aggregate formation in peripheral blood mononuclear cell (PBMC) suspensions depended on cell donor, murine (m) monoclonal antibody (mAb) specificity and IgG subclass, type of fluorochrome conjugated to the mAb, amount of mAb used for immunostaining, time lapse between fixation of PBMC and flow cytometry, and other, as yet unidentified, factors. Platelets, monocytes, and granulocytes express the polymorphic class IIa IgG receptor (Fc gammaRIIa; CD32). A single amino acid difference, either arginine (R) or histidine (H) at amino acid position 131, underlies differential interaction with mIgG1. Because the Fc gammaRIIa-R131 allotypic form binds mIgG1 well in contrast to Fc gammaRIIa-H131, we studied the frequency of aggregate formation in PBMC suspensions from apparently healthy individuals allotyped for Fc gammaRIIa. The Fc gammaRIIa polymorphism contributed significantly to the frequency of mIgG1-induced cell aggregates, which was highest in Fc gammaRIIa-R/R131 individuals, intermediate in Fc gammaRIIa-R/H131 individuals, and lowest in Fc gammaRIIa-H/H131 individuals. The role of mIgG1-Fc gammaRIIa interactions in aggregate formation was confirmed by blocking Fc gammaRIIa by using F(ab')2 fragments of CD32 mAb. These data document the role of mIgG1 mAb binding by human class IIa IgG receptors in the formation of cell aggregates and show that inhibition of this interaction reduces this technical problem in flow cytometric immunophenotyping.

Antibodies, Monoclonal↗
PubMed1999

Hyperammonemia: regulation of argininosuccinate synthetase and argininosuccinate lyase genes in aggregating cell cultures of fetal rat brain.

Hyperammonemia in the brain leads to poorly understood alterations of nitric oxide (NO) synthesis. Arginine, the substrate of nitric oxide synthases, might be recycled from the citrulline produced with NO by argininosuccinate synthetase (AS) and argininosuccinate lyase (AL). The regulation of AS and AL genes during hyperammonemia is unknown in the brain. We used brain cell aggregates cultured from dissociated telencephalic cortex of rat embryos to analyze the regulation of AS and AL genes in hyperammonemia. Using RNase protection assay and non-radioactive in situ hybridization on aggregate cryosections, we show that both AS and AL genes are induced in astrocytes but not in neurons of aggregates exposed to 5 mM NH4Cl. Our work suggests that the hyperammonemic brain might increase its recycling of citrulline to arginine.

Ammonia↗
PubMed1995

Interaction of LHRH with growth hormone-releasing factor-dependent and -independent postnatal development of somatotrophs in rat pituitary cell aggregates.

Addition of LHRH for 40 h to aggregate cell cultures of 14-day-old rat pituitary significantly decreased the number of [3H]thymidine ([3H]T)-incorporating cells which immunostained for GH protein as well as the number of [3H]T-labelled cells expressing GH mRNA detectable by in situ hybridization with a digoxigenin-labelled riboprobe. The effect at the level of GH protein was seen at a dose of 1 nM LHRH. However, the effect at the GH mRNA level required a higher dose of LHRH (10 nM) or a longer incubation time (64 h). Treatment of the cultures for 40 h with 0.1 nM GH-releasing factor (GRF) provoked a 54% increase in the number of [3H]T-labelled cells containing GH mRNA and a 30% increase in the number of cells immunostained for GH protein. The latter effects of GRF were completely blocked by simultaneous addition of LHRH (1 nM) to the cultures. In the absence of GRF, LHRH (1 nM) also had an inhibitory effect on the total number of cells containing GH mRNA and a comparable effect on the total number of cells stained for GH protein. The present data show that LHRH is capable of inhibiting the GRF-independent as well as the GRF-dependent development of somatotrophs in postnatal rat pituitary in culture.

Animals↗
PubMed1976

Cellular composition of erythropoietic cell populations and aggregate cell cultures derived from early chick blastodiscs.

Light and electron microscopy of suspensions of cells prepared by dispersing chick blastodiscs at primitive-streak and head-fold stages showed the presence of numerous yolk granules, yolk-rich endodermal cells and occasional presumed ecto- and mesodermal cells. Several cell fractions prepared from this suspension by sedimentation through discontinuous Ficoll gradients were of similar composition. No enrichment of any particular cell type which might account for either differential sedimentation or erythropoietic potential of the fractions could be recognized. Two fractions, EP 1, and EP 2, were cultured as cell aggregates on vitelline membranes. EP 1 produced highly organized blood islands containing developing erythrocyte cells, organized endothelium, fibroblasts, thrombocytes and occasional granulocytes. Blood islands derived from EP 2, on the other hand, contained essentially only aggregates of erythroblasts embedded in endoderm. It is tentatively suggested that EP1 contains young multipotential hematopoietic precursors while EP 2 has only older blood-cell precursors committed to erythrocyte development. No cellular basis for the resolution of EP 1 into two complementary subfractions could be recognized.

Animals↗
PubMed1976

Red-cell aggregation and red-cell deformability in diabetes.

The anomaly of the viscosity of human blood is more pronounced in diabetics. This is caused by an increase in plasma viscosity, a more pronounced red-cell aggregation, and a reduction of individual cell deformability. The changes in viscosity and in red-cell aggregation both are the consequence of abnormal plasma proteins, the incidence of which is largely independent of the onset and duration of disease, and actual metabolic state. The presence of complicating infectious diseases further aggravates the pathologic red-cell aggregation. The decreased red-cell deformability is largely independent on onset, duration, and complications but depends critically in the incident metabolic control of the diabetics. The possible role of hemorrheologic factors in the development of microangiopathy is discussed.

Blood Proteins↗
PubMed1975

Inhibition of embryonic cell aggregation by neoplastic cells.

The effects of normal and malignant cells on the aggregation of embryonic cells in gyratory shaker cultures were compared. The addition of 1 times 10-5 simian virus 40 (SV40)-transformed BALB/3T3 (SV40-3T3) cells to 6 times 10-6 embryonic neural retina cells caused a highly significant greater reduct on (22.7 percent) in aggregate diameter than the addition of untransformed BALB/3T3 (3T3) cells. The ratio of the number of single cells to the number of aggregates was significantly higher for cultures containing SV40-3T3 cells than for the cultures containing 3T3 cells. This effect was concentration dependent in the presence of cultured Ehrlich-Lettre hyperdiploid (ELD) ascites cells; however, media from ELD cell cultures or ELD cell sonicates resulted in aggregates of greater diameter and lower ratios of single cells to aggregates. This approach may provide a sensitive assay system for the interactions of tumor and other cells in vitro.

Animals↗
PubMed1976

Differential inhibition of embryonic cell aggregation by cultured human cells with "malignant" of "normal" characteristics.

The effect that cultured human cells have on chick embryonic neural retina cell aggregation was examined. Different types of human cultured cells inhibited aggregation of chick neural retinal cells to differetn degrees when mixed at a human cell:retina cell ration of 1:60. It appeared from the eleven cell lines studied that cells with "malignant" characteristics inhibited retinal cell aggregation to a greater extent than those with more "normal" characteristics. The assay could be used as a further test for abnormality of cell types and also as a method for studying the interactions of malignant cells with cultured cells.

Cell Aggregation↗
PubMed1983

Ultrastructural and protein synthetic changes in embryonic brain: cells aggregated at 0 degree C.

Cells dissociated from brains of 16 to 18 day-old mice embrya were rotated at 37 degrees C and 0 degree C for 7--8 days. While cells aggregated at 37 degrees C formed compact aggregates, cells aggregated at 0 degree C were found in clusters or were randomly distributed. Cells aggregated in the cold did not differ markedly from the controls in their ultrastructural organisation till the 2--3 day in vitro (DIV). Later, significant structural changes, such as distention of cytoplasmic membranes, destruction of mitochondrial membranes, disappearance of ribosomes, shrinkage of nuclei and disturbance of cytoplasmic membranes were apparent. On the 6--7 DIV, groups of cells were separated by a distance of 100 nm and more, and large parts of their cytoplasm disappeared and outside cell perikarya fragments of membranes appeared forming dense debris. However, even at this period some cells were found which did not show signs of degeneration. Protein synthetic activity in aggregated cells increased linearly at 37 degrees C till 7 DIV, whereas in cells aggregated at 0 degree C an inhibition of about 34% was found at 4 DIV and at 7 DIV the curve of 14C leucine incorporation declined almost to zero. It is thus evident that cells aggregated at 0 degree C maintain an almost normal ultrastructural pattern during the first days of cultivation and only protein synthetic activity is lowered. Cellular membranes, damaged during the dissociation partly regenerated even at 0 degrees C and membraneous contacts were formed between several cells.

Animals↗
PubMed2006

Phenylpropanoid metabolite supports cell aggregate formation in strawberry cell suspension culture.

Plant cells in suspension culture tend to aggregate and form large clumps. In suspension culture, large cell aggregates are frequently subjected to hydrodynamic shear stress; however, a certain degree of cell aggregation is often required for cell growth and metabolite production. Thus, controlling cell-aggregate size is desired to establish high productivity of useful products using plant cell suspension culture. In this study, we focused on the relationship between cell-aggregate formation and secondary metabolism. We found that anthocyanin concentration showed a good correlation with cell-aggregate size in the cultured strawberry cell line FAR (Fragaria ananassa R), which produces anthocyanin and other phenylpropanoid metabolites constitutively without illumination. This result suggests that there is a relationship between cell-aggregate formation and the accumulation of phenylpropanoid metabolites. To investigate the direct effect of phenylpropanoid metabolism on cell-aggregate formation, the time course of cell-aggregate size was monitored when phenylpropanoid metabolism was suppressed by a metabolic inhibitor, L-alpha-aminooxy-beta-phenylpropionic acid (AOPP), a specific inhibitor of phenylalanine ammonia lyase which is the starting and key enzyme of the phenylpropanoid pathway. In the absence of AOPP, the average diameter of cell aggregates increased on day 8 of culture. This increase in cell-aggregate size was completely suppressed by the addition of 0.1 mM AOPP, without any reduction in cell growth rate or soluble protein content. These results indicate that cell-aggregate formation is directly supported by a secondary metabolite produced from the phenylpropanoid pathway, suggesting that cell-aggregate size can be controlled by AOPP without inhibition of primary metabolism.

Anthocyanins↗
PubMed1982

General inhibition of embryonic cell aggregation by neoplastic cells.

The presence of small numbers of cancer cells cause an inhibition in the aggregation of embryonic chick neural retina cells. Experiments were made to investigate the inhibitory action of malignant mouse and virus-transformed chick neural retina cells on the aggregation and adhesion of several embryonic cell types. Malignant mouse cells, and their conditioned medium, inhibited the aggregation and adhesion of embryonic skeletal muscle heart and liver cells. The transformed retinal cells inhibited the aggregation of neural retina cells. These results suggest that the effect of cancer cells on the behavior of embryonic cells is a general one not related to the origin of the cancer cells.

Animals↗
PubMed1983

Evidence for paracrine interaction between gonadotrophs and lactotrophs in pituitary cell aggregates.

Pituitary cell aggregates prepared from 14-day-old male or female rats and maintained for 4-5 days in culture were superfused with LHRH during periods of 20 or 90 min. LHRH provoked a rapid and sustained rise of PRL release at concentrations similar to those stimulating LH release (10(-11)-10(-8) M). Dopamine, at a concentration inhibiting PRL release for 90%, weakened but did not prevent this stimulation. LHRH also stimulated PRL release in aggregates prepared from adult male rat pituitary cells, but the effect was weaker and seen only after a more prolonged period in culture. There was no PRL response to LHRH in aggregates of lactotroph-enriched populations, obtained by gradient sedimentation at unit gravity, in which only few and small gonadotrophs are present. When a lactotroph-enriched/gonadotroph-poor population was coaggregated with a highly enriched population of large gonadotrophs, LHRH very effectively stimulated PRL release, the extent of stimulation being dependent on the proportional number of gonadotrophs in the coculture. Superfusion of lactotroph-enriched/gonadotroph-poor aggregates with medium in which the gonadotroph-enriched aggregates had previously been incubated for 3 h with 1 nM LHRH (gonadotroph-conditioned medium) also provoked a clear-cut rise in PRL release. This effect was not due to LH, FSH, or the small amounts of PRL present in the gonadotroph-conditioned medium. The LHRH antagonist [D-Phe2-D-Ala6]LHRH was capable of blocking the PRL response to LHRH but not that to the gonadotroph-conditioned medium. In the lactotroph-gonadotroph coaggregates TRH stimulated PRL release but had no effect on LH release. TRH was also ineffective in releasing LH or FSH in populations containing both gonadotrophs and thyrotrophs. The present data suggest that gonadotrophs can activate the secretory activity of the lacotrophs through the release of a paracrine humoral factor.

Animals↗
PubMed2006

Estradiol induces expression of 5-hydroxytryptamine (5-HT) 4, 5-HT5, and 5-HT6 receptor messenger ribonucleic acid in rat anterior pituitary cell aggregates and allows prolactin release via the 5-HT4 receptor.

Serotonin [5-hydroxytryptamine (5-HT)] is known to control prolactin (PRL) release at a hypothalamic level, but a pituitary site of action remains poorly studied. The present study explores the acute effect of 5-HT on PRL release in rat anterior pituitary aggregate cell cultures, the influence of steroid and thyroid hormones, and the 5-HT receptor (5-HTR) subtype(s) involved. 5-HT elicited a prompt increase in basal PRL release, an effect strongly potentiated by estradiol (E(2)) in the culture medium (dose response 1-100 nm). In E(2) condition, the PRL response was not affected by the nonselective 5-HTR antagonists methysergide and methiothepin nor by 5-HTR1, 5-HTR2, 5-HTR3, 5-HTR6, and 5-HTR7/5 antagonists, but was fully blocked by the 5-HTR4 antagonist GR 113808. Among various agonist analogs, only the 5-HTR4 agonist cisapride and the 5-HTR2 agonist alpha-methyl-5-HT evoked PRL release. The effect of alpha-methyl-5-HT also required E(2) during culture and was abolished by GR 113808 but not by combined 5-HTR2A, B, and C blockade. In E(2)-treated aggregates, 5-HT caused a 5-fold increase in cAMP levels. The intact anterior pituitary expressed mRNA of all known members of the 5-HTR family. In aggregates, 5-HTR4, 5-HTR5, and 5-HTR6 mRNA expression required E(2) during culture. The effect of 5-HT on PRL release was not affected by blocking the serotonin transporter or the vesicular monoamine transporter. The present data suggest a widespread expression of 5-HTRs in the rat anterior pituitary, several of which are up-regulated by estrogen, and that, in the presence of estrogen, one of these, the 5-HTR4, mediates acute PRL release.

Animals↗