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At least 127 records · Page 7Linked to original sources
PubMed1975

Stimulation of HeLa-S3 cell aggregation by sugars related to cell membrane in rotation culture.

Effect of various sugars related to cell membrane on the aggregation of HeLa-S3 cells was examined in a rotation culture by adding each sugar to the culture medium. Some specific sugars among those tested induced (1) greater size of aggregates and (2) higher synthesis of hyaluronic acid than that of the control. Since the addition of hyaluronidase inhibited the aggregate formation, both in the test and control cultures, with HeLa-S3 cells of both groups forming only small aggregates, it was presumed that the hyaluronic acid synthesized might be of cardinal importance for the formation of aggregates. The specific sugars producing the effect mentioned above were N-acetyl-D-glucosamine, bis(N-acetyl)chitobiose, N-acetyl-D-galactosamine, alpha-methyl-D-glucopyranoside, and N-acetyl-D-mannosamine, while D-glucosamine, beta-methyl-D-glucopyranoside, L-fucose, D-glucose, and a commercially available hyaluronic acid were ineffective. The findings obtained in the present study interestingly ran parallel with the results of previously reported study on the induction of specific biological phenomena by the cell membrane-related sugars.

Acetylgalactosamine↗
PubMed1997

Anti-CD53 monoclonal antibody induced LFA-1/ICAM-1-dependent and -independent lymphocyte homotypic cell aggregation.

CD53 is a pan-leukocyte glycoprotein and belongs to a member of the tetraspan family of cell membrane proteins. The predicted structure and functional characteristics of CD53 suggest that it may play important roles in transmembrane signaling, but its roles in cell adhesion have not been clarified. The present study shows that anti-CD53 monoclonal antibody (mAb), HI29 induced homotypic cell aggregation of lymphoid cell lines including a B cell line from a patient with leukocyte adhesion deficiency syndrome (LAD). The homotypic cell aggregation was blocked by another anti-CD53 mAb, MEM53, in all the examined cell lines and by anti-LFA-1 (CD11a/CD18) or anti-ICAM-1 (CD54) mAbs in the cell lines except for the LAD line, but it was not blocked by anti-CD44 or anti-CD49d mAb. The induced homotypic cell aggregation was energy-dependent. These findings suggest that CD53 relates to LFA-1/ICAM-1-dependent and -independent pathways of homotypic cell aggregation of lymphocytes and that it plays an important role in lymphocyte activation and cell adhesion.

Antibodies, Blocking↗
PubMed1992

R1-20, a novel monoclonal antibody reacting with a molecule distinct from integrin family, induces homotypic cell aggregation.

R1-20, a novel mAb reacting with a cell surface Ag on normal human lymphocytes and leukemic cell lines, was shown to induce homotypic cell aggregation in leukemic cell lines. This phenomenon was specific to mAb R1-20 because antibodies recognizing CD2, CD7, CD28, and HLA-ABC failed to exhibit homotypic cell aggregation. Induction of aggregation by mAb R1-20 occurred at 37 degrees C, but not at 4 degrees C and required cytoskeletal integrity. Sodium azide, a metabolic inhibitor, had no effect on the aggregation. Distinct from lymphocyte function-associated Ag-1/intercellular adhesion molecule-1 interaction in which divalent cations are essential elements, R1-20-mediated aggregation was not abolished with EDTA treatment. The R1-20 Ag was determined as a molecule of M(r) 100 to 110 kDa in immunoprecipitation and immunoblotting methods, under both reducing and nonreducing conditions. The molecular composition is quite different from that of any known integrin molecule. The R1-20 Ag was expressed on resting and activated T Lymphocytes as well as on normal B lymphocytes. Monocytes and granulocytes had no detectable R1-20 Ag. Among the leukemia-derived cell lines we used, mAb R1-20 reacted with 18 of 32 T cell lines, 2 of 20 B cell lines, 2 of 3 non-T-non-B cell lines, 2 of 7 myelomonocytic cell lines, and 2 of 3 nonlymphoid-nonmyeloid cell lines. All EBV-transformed B cell lines examined (10 cell lines) were R1-20+. The spectrum of reactivity among the cell lines tested was different from that of known antiadhesion antibodies tested. All these findings indicate that the Ag recognized by mAb R1-20 may represent a new type of cell adhesion molecule.

Antibodies, Monoclonal↗
PubMed2003

Cell aggregation precedes the onset of Sox9-expressing preSertoli cells in the genital ridge of mouse.

SOX9 is expressed at the onset of the genital ridge formation in both sexes. It is assumed that SRY, the testis determining gene, turns SOX9 on in male embryos because it is turned off in female embryos. Spatial expression of SRY follows a cranio-caudal pattern. Here, we asked if SOX9 is expressed in the same cell lineage and with a similar pattern as SRY. A correlative study between the structural changes in the genital ridge and the immunocytochemical localization of SOX9-positive cells was undertaken. We used a transgenic strain expressing the green fluorescent protein (GFP) that considerably enhanced the cell context where the first SOX9-positive cells appear. Although SOX9-positive cells are located among loose mesenchymal cells by stages of 8-14 tail somites (ts) in both sexes, they are absent in the thickening coelomic epithelium of females. At 15 ts the first SOX9-positive cells appear within the core of the condensed cells only in male genital ridges. At 17 ts, a gradient of SOX9-positive cells in males is apparent, closely following the cranio-caudal pattern of cell aggregation seen in genital ridges of both sexes. Hence, our results suggest that SOX9 is expressed only in loose mesenchymal cells in both sexes and that expression of SOX9 in males requires the prior aggregation of cells in the genital ridges. The correspondence of SOX9 and SRY pattern of expression supports that both genes are expressed in the preSertoli cell lineage in the core of the genital ridges.

Animals↗
PubMed1999

cAMP levels in cells attached to AN69 and Cuprophan: cAMP dependence of cell aggregation and the influence of serum.

We have examined the link between the aggregation or spreading of cells adhering to substrata of differing biocompatibility and activation of the cyclic AMP (cAMP) pathway. We compared the rate at which the Mouse Swiss 3T3 fibroblasts attached to Cuprophan (CU), AN69 and a control plastic in the presence and absence of foetal calf serum (FCS). Serum had no effect on the kinetics of cell attachment to CU or AN69. Cells incubated in culture medium containing 10% FCS aggregated on CU, whereas they spread on AN69 and plastic. Aggregated cells contained significantly higher concentrations of cAMP than cells spreading, and aggregation was prevented by treatment with miconazole, an inhibitor of adenylyl cyclase. cAMP-dependent cell aggregation occurred on all three substrata in serum-free medium, suggesting that proteins adsorbed onto AN69 and plastic in the presence of serum helped protect the cells. Far less serum protein was adsorbed onto CU than onto AN69 or plastic, consistent with the similar increases in cAMP in cells attached to CU with or without serum.

3T3 Cells↗
PubMed2003

Cell and organ printing 2: fusion of cell aggregates in three-dimensional gels.

We recently developed a cell printer (Wilson and Boland, 2003) that enables us to place cells in positions that mimic their respective positions in organs. However, this technology was limited to the printing of two-dimensional (2D) tissue constructs. Here we describe the use of thermosensitive gels to generate sequential layers for cell printing. The ability to drop cells on previously printed successive layers provides a real opportunity for the realization of three-dimensional (3D) organ printing. Organ printing will allow us to print complex 3D organs with computer-controlled, exact placing of different cell types, by a process that can be completed in several minutes. To demonstrate the feasibility of this novel technology, we showed that cell aggregates can be placed in the sequential layers of 3D gels close enough for fusion to occur. We estimated the optimum minimal thickness of the gel that can be reproducibly generated by dropping the liquid at room temperature onto a heated substrate. Then we generated cell aggregates with the corresponding (to the minimal thickness of the gel) size to ensure a direct contact between printed cell aggregates during sequential printing cycles. Finally, we demonstrated that these closely-placed cell aggregates could fuse in two types of thermosensitive 3D gels. Taken together, these data strongly support the feasibility of the proposed novel organ-printing technology.

Animals↗
PubMedDate not supplied

Infiltration and lysis of tumour cell aggregates by adherent interleukin-2-activated natural killer cells is distinct from specific cytolysis.

Adoptively transferred activated natural killer (A-NK) cells infiltrate tumours in vivo. Two in vitro B16-F10 melanoma tumour models were used to study with fluorescence and electron microscopy the infiltration of adherent interleukin 2 (IL-2) A-NK cells: (1) substratum-bound sessile microtumours (MTs), and (2) three-dimensional cell growth on macroporous gelatinous microcarriers (Cultispheres). From 2 h and on increasing numbers of A-NK cells infiltrated the MTs regularly surrounded by a widened intercellular space. An IL-2-dependent disintegration of MTs began at 6-8 h resulting in a release of vital and dead cells. A-NK cell invasion into Cultispheres effectively displaced the melanoma cells from the highly convoluted substratum. Thus, A-NK cell infiltration had a protease-like effect on the tumour cell aggregates which might have a bearing on the interpretation of their cytolytic effect on target cells. Ultrastructural evidence was not obtained of specific A-NK/target conjugate formation or of granule-mediated target cell destruction in either model tumour.

Adoptive Transfer↗
PubMed1999

Recombinant protein synthesis in Trichoplusia ni BTI-Tn-5B1-4 insect cell aggregates.

The Trichoplusia ni BTI-Tn-5B1-4 (Tn-5B1-4) insect cell line has received considerable attention as a host for the baculovirus expression vector system. In the present study, suspension cultures were used to compare Tn-5B1-4 cell aggregates and cells selected to grow predominantly as individual cells. No significant difference was found between cell aggregates and cells growing predominantly individually in regard to cell growth rate, glucose consumption and lactate accumulation, and specific recombinant protein synthesis levels. In addition, the levels of recombinant protein synthesis were considerably higher than those produced by the commonly used Spodoptera frugiperda Sf-9 insect cell line.

Alkaline Phosphatase↗
PubMed2002

[Relation between formation time and structure of red blood cell aggregation body]

OBJECTIVE: To study the relation between of forming time red blood cell aggregation body and structure by changing the thickness of flow channel plane and red blood cell hematocrit. METHODS: A system with flow channel technique and light transmission measurements were applied to gaining red blood cell aggregation curve. RESULTS: The forming time of red blood cell aggregation body and the thickness of aggregation body as well as red blood cell hematocrit were linearily correlated with a correlation coefficient gamma of 0.989 and 0.990 respectively. CONCLUSION: When red blood cell aggregation process is studied using different methods, red blood cell aggregation time index can not be compared.

Journal Article↗
PubMed2004

Abnormal Leydig Cell aggregation in the fetal testis of rats exposed to di (n-butyl) phthalate and its possible role in testicular dysgenesis.

Fetal exposure of male rats to di (n-butyl) phthalate (DBP) induces testicular changes remarkably similar to testicular dysgenesis syndrome in humans; these include induction of focal areas of dysgenetic tubules in otherwise normal testes. In searching for the fetal origins of the latter, we used image analysis to show that exposure to 500 mg/kg DBP [embryonic day (E)13.5-20.5)] caused abnormal aggregation of Leydig cells centrally in the fetal testis. This aggregation was not due to increase in Leydig cell number, and Leydig cell size was significantly reduced in DBP-exposed animals, as were testosterone levels and immunoexpression of P450 side-chain cleavage enzyme. The Leydig cell aggregates did not exhibit evidence of focal proliferation at E17.5-19.5. Using confocal microscopy and Leydig (3beta-hydroxysteroid dehydrogenase) and Sertoli (anti-Mullerian hormone) cell-specific markers, we show that fetal Leydig cell aggregates in DBP-exposed animals trap isolated Sertoli cells within them at E21.5. These areas of intermingled cells are still apparent on postnatal d 4, after cessation of DBP treatment, when they may form misshapen seminiferous cords that trap (intratubular) Leydig cells within them. These centrally located dysgenetic tubules contain germ cells in early puberty, but by adulthood they are Sertoli cell only, implying that presence of intratubular Leydig cells interferes with spermatogenesis. It is concluded that DBP-induced fetal Leydig cell aggregation may be a key event in formation of focal dysgenetic areas in the testis, and identification of the mechanisms underlying these events may give new insights into the fetal origins of testicular dysgenesis syndrome disorders in the human.

Abnormalities, Drug-Induced↗
PubMed1978

A collision analysis of lymphoid cell aggregation.

We have obtained data on the frequency of aggregates of different size classes and on the maximum aggregate diameter of lymphoid cells subjected to aggregation in the laminar shear field of a Couette viscometer. Maximum aggregate diameter reached a plateau level during aggregation. This plateau is considered to be the result of a balance between the hydrodynamic shear forces tending to resist the formation of aggregates, and the adhesive forces of the aggregated cells tending to resist dissociation. Stepwise-increases in the shear rate produced aggregates of progressively smaller maximum diameter until the limiting (i.e. control equivalent) diameter was reached. Equations governing these stepwise changes in aggregate diameter were obtained by regression analysis, and an estimate of the force of dissociation (FD) was made from derived values of the critical shear rate. Thymocytes (FD=2.54 X 10(-6) N m-2/cell) were found to be more adhesive than lymphocytes (FD=2.05 X 10(-6) N m-2/cell), in agreement with current concepts. The observed data on aggregate frequency were seen to be of poor fit with a model of aggregation derived by collision analysis of the aggregation process. This led us to consider the possibility that all cells may not share the same probability of forming an adhesion. We thus derived further models of aggregation in which some fraction of the total cells was considered to have enhanced possibilities of a collision producing an adhesion. Of the models we considered, a 15% preferred fraction offered best agreement with the experimental observations. We therefore conclude that the populations of cells studied in this report are not 'homogenous' in that some cells are more adhesive than others. Alterations in the percentage of the preferred fraction of cells will lead to different aggregate-frequency indices. Such changes might be expected to occur during the initial stages of carcinoma development.

Animals↗
PubMed1997

Bursting behavior during fixed-delay stimulation of spontaneously beating chick heart cell aggregates.

Spontaneously beating embryonic chick atrial heart cell aggregates were stimulated with depolarizing current pulses delivered at a fixed delay after each action potential. This preparation is an experimental model of a reentrant tachycardia. During fixed-delay stimulation, bursting behavior was typically observed for a wide range of delays. Episodes of bursting at a rate faster (slower) than control were followed by overdrive suppression (underdrive acceleration). We use a simple nonlinear model, based on the interaction between excitability and overdrive suppression, to describe these dynamics. A modified version of the Shrier-Clay ionic model of electrical activity of the embryonic chick heart cell aggregates that includes a simplified Na+ pump term is also presented. We show that the complex patterns during fixed-delay stimulation arise as a result of delicate interactions between overdrive suppression and phase resetting, which can be described in terms of the underlying ionic mechanisms. This study may provide a basis for understanding incessant tachycardias in the intact heart, as well as an alternative mechanism for the emergence of bursting activity in other biologic tissue.

Action Potentials↗
PubMed1983

Sorting out in heterotypic cell aggregates is regulated by differences in the cell surface charge.

Random aggregates of heterotypic cells derived from two different embryonic tissues sort out into homotypic zones, one enclosing the other. The specification of the enclosed or enclosing position is based on a tissue hierarchy. Cells differ in their net negative charge as indicated by their different isoelectric points (pI). The cells of higher pI enclose the cells of lower pI. Cell pI is lowered by treatment with heparin. Cells with experimentally altered pI also sort out, and their position is specified by the differences in their pI. It is suggested that the cell surface ionogenic groups determine the free surface energy which controls the positioning of cells in a mixed aggregate.

Animals↗
PubMed1992

Increased red cell aggregation does not reduce uteroplacental blood flow in the awake, hemoconcentrated, late-pregnant guinea pig.

The effect of increased red blood cell aggregation on uteroplacental blood flow was studied in 11 awake, late-pregnant guinea pigs. The aggregation of the red cells was increased by administering high molecular weight dextran (HMWD) to the previously hemoconcentrated animal. The purpose of the hemoconcentration before HMWD was 1) to use a preeclampsia model in which the hemorheology may be impaired because of the combined effect of polycythemia, an increased red cell aggregation, and an increased plasma viscosity and 2) to potentiate the aggregation-increasing effect of HMWD. Relative to the pre-HMWD condition, arterial blood pressure and systemic vascular resistance increased by 10 and 26%, respectively. The cardiac output fraction shunted across the systemic circulation and the arterial hematocrit decreased by 30 and 4%, respectively. Neither cardiac output nor the weighted organ flows, including those to the placentas, changed in response to the rise in red cell aggregation. We conclude that an imposed increase in red cell aggregation has no appreciable effect on uteroplacental blood flow in the awake and healthy late-pregnant guinea pig. These data do not exclude the possibility that increased red blood cell aggregation potentiates the negative effects on uteroplacental blood flow, e.g. in pregnancy-induced hypertension or preeclampsia, where the placenta is not only marginally perfused but also frequently damaged histologically.

Animals↗
PubMed1983

Red cell aggregation as a cause of blood-flow echogenicity.

The role of red cell aggregation as a cause of ultrasonic echogenicity in flowing blood was evaluated by in vitro experiments using fresh human blood. Blood was circulated in tubes of varying diameter (12 mm to 6 mm). In all experiments, echogenicity increased as blood approached static conditions. Echogenicity was greater in tubes with a larger diameter over the same range of blood velocity. However, echogenicity in tubes of various diameters was the same when evaluated in terms of shear rate. Thus, shear rate and not velocity is the flow condition that determines echogenicity. Since shear rate determines the degree of red cell aggregation, while other conditions affecting red cell aggregation (hematocrit, erythrocyte membrane conditions, and plasma macromolecules) are held constant, we conclude that these results provide additional evidence that red cell aggregation is a cause of echogenicity in flowing blood. Furthermore, a red cell aggregation mechanism for blood-flow echogenicity would explain the increased prominence of internal echoes in lower shear rate venous blood flow compared with those of higher shear rate arterial blood flow.

Cardiovascular Physiological Phenomena↗
PubMed1986

Roles of surface electrochemistry and macromolecular adsorption in heparin-induced red blood cell aggregation.

Red blood cell (RBC) aggregation in heparin-saline solution was quantified by microscopic observation. The adsorption isotherms of heparin onto normal and neuraminidase-treated RBC surfaces were determined by radioactive heparin labeled with 125I-Bolton-Hunter Reagent. RBC aggregation by heparin requires the presence of sialic acids at cell surface and was enhanced by reduction of ionic strength of the suspending medium. Adsorption of heparin onto RBC surface was increased by removal of sialic acids. These findings not only serve to elucidate the basic mechanism of cell-cell interaction mediated by negatively charged macromolecules, but also provide experimental evidence for the possible conformational change of macromolecules at the charged surface.

Adsorption↗
PubMed1976

Isolation of retina-specific cell-aggregating factor from membranes of embryonic neural retina tissue.

There is increasing evidence that developmental associations among embryonic cells are mediated by specific components of the cell surface. Earlier work has indicated that such components are extruded into the medium of primary monolayer cultures of embryonic cells, and that they represent the active constituents of the tissue-spedific cell-aggregating factors isolated fro- the supernatant medium of such cultures. We presently report that tissue-specific cell-aggregating factors can be obtained directly from embryonic tissues, and describe the isolation and partial purification of retina-spedific factor from a cell-membrane preparation derived from retina tissue of the chick embryo. Extraction of the purified membrane preparation with 1-butanol yielded an activity in the aqueous phase which resides in a protein probably a glycoprotein, with an estimated molecular weight of 50,000 in solution. This material could be obtained from retinas of embryos not older than 13 days, and only pre-13-day cells responded to its cell-aggregating activity. By these characteristics, this membrane-derived retina factor closely resembles the retina cell-aggregating glycoprotein previously purified from the supernatant medium of retina cell cultures. It is of special interest that the cell-aggregating protein is obtainable from cellular membranes during those stages of development when retina cells are most actively engaged in histological organization. Work in progress indicates that, by the procedures described herein, tissue-specific cell-aggregating factors can also be obtained from membrane preparations of other embryonic tissues.

Age Factors↗