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Cell-cell interactions during neural development: multiple types of lateral inhibitions involved in Drosophila eye development.

Inhibitory signals of cellular differentiation from differentiating cells play an important role in regulating the number and spatial distribution of distinctive types of cells in developing tissues. Several types of inhibitory mechanisms of cellular differentiation have been identified by making full use of the developmental genetics of Drosophila compound eyes. These inhibitory mechanisms are distinct from each other in their signal transduction cascades and/or their role in the pattern formation of the developing Drosophila eye. The following events occur: firstly a diffusible protein, Scabrous (Sca), is required to confer regular spacings of the founder cells, R8 cells, or preommatidial clusters in the developing eye disc via an unknown signal transduction cascade, secondly the Notch-signalling is at least required for the single-out of the R8 cells within the pre-ommatidial cluster possibly by preventing other cells in the equivalent groups from adapting fates as R8 cells. Notch-signalling activates a simple signal cascade mediating communication between the plasma membrane and nucleus not via protein phosphorylation. In contrast, a novel diffusible ligand, Argos, was likely to be required subsequently to the selection of R8 cells. Argos was shown to inhibit the activation of a receptor tyrosine kinase, DER, and the subsequent signal transduction in the Ras/MAPK cascade (the third inhibitory mechanism). We proposed that the role of Argos is to regulate the number of differentiated cells by controlling cellular differentiation and subsequent programmed cell death. The distinct roles of these inhibitory signals in the developing Drosophila eye are discussed in detail.

Animals↗

Stromal-epithelial interactions in aging and cancer: senescent fibroblasts alter epithelial cell differentiation.

Cellular senescence suppresses cancer by arresting cells at risk of malignant tumorigenesis. However, senescent cells also secrete molecules that can stimulate premalignant cells to proliferate and form tumors, suggesting the senescence response is antagonistically pleiotropic. We show that premalignant mammary epithelial cells exposed to senescent human fibroblasts in mice irreversibly lose differentiated properties, become invasive and undergo full malignant transformation. Moreover, using cultured mouse or human fibroblasts and non-malignant breast epithelial cells, we show that senescent fibroblasts disrupt epithelial alveolar morphogenesis, functional differentiation and branching morphogenesis. Furthermore, we identify MMP-3 as the major factor responsible for the effects of senescent fibroblasts on branching morphogenesis. Our findings support the idea that senescent cells contribute to age-related pathology, including cancer, and describe a new property of senescent fibroblasts - the ability to alter epithelial differentiation - that might also explain the loss of tissue function and organization that is a hallmark of aging.

Animals↗

An epigenetic model for the origin of cancer.

A unifying concept that appears to provide an understanding of cancer as a fundamental scientific problem is presented. This concept, which was initially developed on the basis of experiments using the relatively uncomplicated plant tumor systems, now appears applicable to animal and human tumors as well. Evidence is provided to show that the tumor problem is fundamentally a problem of anomalous cellular differentiation and that the heritable cellular change that underlies the tumorous state is similar to that which underlies cell specialization occurring during the normal course of development in all higher organisms. Both cellular differentiation and tumorigenesis depend for their expression on the persistent activation of select but, in part, different genes (whether normal, foreign, or both) present in the genome of a cell. Since heritable cellular changes of this kind may be induced by physical, chemical, and biological agents of the most diverse type, and since cells may remain totipotent during the time that they exhibit the tumor phenotype, the results reported here suggest that whether the normal or tumor phenotype is expressed is determined by how the genetic information present in a cell is regulated in the cell. Regulation leading to the establishment and maintenance of the tumorous state may be accomplished in different ways by the different types of oncogenic agents. Thus cancer and related neoplastic diseases appear to have a common underlying heritable cellular change in which the diverse manifestations of the tumorous state commonly observed would simply reflect different expressions of this heritable cellular change.

Animals↗

Effect of nerve growth factor and forskolin on glycosyltransferase activities and expression of a globo-series glycosphingolipid in PC12D pheochromocytoma cells.

The glycosphingolipid (GSL) composition of cells changes dramatically during cellular differentiation. Nerve growth factor (NGF) or forskolin (FRK) are known to induce cellular differentiation including process formation in PC12 pheochromocytoma cells. In this respect, we present the NGF/FRK-dependent regulation of glycosyltransferase activities and the corresponding GSL expression in PC12D cells. After treatment of PC12D cells with NGF or FRK, the cell processes, including varicoses and growth cones, became strongly immunoreactive with an antibody against a unique globo-series neutral GSL, Gal alpha 1-3Gal alpha 1-4Gal beta 1-4Glc beta 1-1'Cer (GalGb3), and the activity of GalGb3-synthase increased significantly. Other glycosyltransferase activities, including GM1 containing blood group B determinant (BGM1)-, GM3-, GD1a-, and GM2-synthases, also increased significantly upon NGF treatment, but the immunoreactivity against BGM1 did not show any appreciable change. For the parent PC12 cells, NGF/FRK treatment significantly increased the percentage of anti-GalGb3 positive cells and induced some immunoreactive cell processes. Because the parent PC12 cells do not express appreciable amounts of GalGb3, and because PC12D cells are considered to be more differentiated than the parent PC12 cells, the expression of GalGb3 and the increase of GalGb3-synthase activity may be closely related to the cellular differentiation process in this cell line.

Animals↗

[Multiparametric cytofluorometry of the process of cellular proliferation, differentiation and maturation of the chondrocytes in the growing rat].

The present study was undertaken to analyze quantitatively the process of cellular proliferation, differentiation and maturation of the chondrocytes in both the epiphyseal cartilage plates and the articular cartilages of the growing rats, using the multiparametric cytofluorometry (NIKON SPM-RFl-D). The analyses involve the simultaneous determinations by cytofluorometry of nuclear DNA vs. cellular RNA contents, nuclear DNA vs. cellular protein contents, and nuclear DNA vs. silver grain amount of the 3H-leucine, 3H-glycine, 3H-thymidine and the 35SO4 autoradiography. In addition, for the detailed analysis of cell kinetics, DNA-RNA cytofluorometry was carried out in combination with 3H-thymidine autoradiography. According to the results obtained, the chondrocytes were quantitatively divided into subpopulations of G0-G1, S and G2 in the cell cycle by their nuclear DNA and cellular RNA contents, and the maturative chondrocytes had higher cellular RNA content than the proliferative ones. It was suggested that there were, among the chondrocytes in the epiphyseal cartilage plate, two other subpopulations of binuclear cells and mononuclear tetraploid cells, both having higher cellular RNA content than the mononuclear G2 cells. It is reasonable to assume that these two subpopulations are the polyploid cell groups accompanying highly active cell proliferation.

Animals↗

Molecular aspects of lens cell differentiation.

I have presented a series of observations on macromolecular interactions which occur during the terminal stages of lens cell differentiation. These are summarized in Fig. 2. Other cell types that undergo similar changes are the erythrocyte and skin cells (epidermis) during the process of keratinization. These other cells are also involved in the synthesis of highly specific proteins, and there are indications that molecular alterations similar to those described for the lens may also occur in these cells (26). Thus, elucidation of a specific series of macromolecular initeractions such as those described may provide a basis for the biochemical definition of the terminal stages of cellular differentiation. Differentiation of the reticulocyte, for example, involves inactivation of the nucleus, stabilization of mRNA, and possibly a ribosomal breakdown such as I have described here (26). Furthermore, elucidation of the mechanisms of reactions involving the initiation of tissue-specific protein synthesis and suLbsequent nuclear inactivation, stabilization of mRNA, and breakdown of the ribosomes may provide a basis for defining the mechanisms of terminal cellular differentiation. The lens cell has reached its highest form of cellular differentiation when it has formed the fiber cell. With respect to the mechanism of lens fiber cell formation, we would like to know whether specific biochemical changes such as gamma-crystallin synthesis are intiniately linked to fiber cell formation-that is, whether gamma-crystallins are required to bring about the formation of a fiber cell. The potential for synthesizing gamma-crystallins is inherent in the genome of the cell. This part of the genome is nonfunctional in the epithelial cell. Can these genes be activated without bringing about a simultaneous cellular elongation, nuclear inactivation and loss of cellular replication, stabilization of mRNA, and breakdown of the ribosomes? The degree of coupling or uncoupling of tissue-specific-protein synthesis to morphogenesis is an important part of the mechanism of cellular differentiation. We feel that we have now reached the stage where we can begin to answer these questions.

Animals↗

[Squamous cell carcinoma of the penis: treatment protocol according to our 14 years of experience].

OBJECTIVE: The management of lymph nodes and the determination of prognostic factors are matters of controversy in the treatment of squamous cell carcinoma of the penis. We attempted to establish an approach based on the different types of lymphadenectomies and biopsies we have performed and to evaluate local stage and grade of cellular differentiation as prognostic factors. METHODS: 81 cases treated at our institution between 1980 and 1994 were reviewed. The results of the different lymphadenectomies and biopsies performed were analyzed. Tumors were staged according to the Jackson and TNM classifications; in 62 cases the pathological samples were reexamined by the same pathologist to determine the grade of cellular differentiation according to the Broders classification. A p value of < 0.05 was considered significant. RESULTS: We did not obtain reliable results with the biopsies done and variable results in the lymphadenectomies performed. The grade of cellular differentiation and local stage were both statistically significant with respect to the presence of positive lymph nodes. We found statistically significant differences for survival according to the stage of the positive lymph nodes. CONCLUSION: We have established three approaches in management of squamous cell carcinoma of the penis according to the local stage and grade of cellular differentiation.

Adult↗

Biological implications of estrogen and androgen effects on androgen receptor and its mRNA levels in human uterine endometrium.

It has been shown that some effects of testosterone are different from those of its 5 alpha-reduced metabolite, dihydrotestosterone. Briefly, activities of testosterone might be related to cellular differentiation, whereas dihydrotestosterone acts on cellular proliferation. The number of testosterone binding sites in the uterine endometrium was increased by estradiol dipropionate, and this increase was down-regulated by testosterone cypionate. Dihydrotestosterone-specific binding sites in the endometrium were not modulated by estradiol dipropionate and testosterone cypionate. The dissociation constants of the binding sites for testosterone and dihydrotestosterone were not altered by these steroids. Estradiol dipropionate with or without testosterone cypionate induced androgen receptor mRNA expression in the endometrium. In conclusion, testosterone might predominantly affect cellular differentiation in the endometrium.

Adult↗

Activation of the Ca(2+)/calcineurin/NFAT2 pathway controls smooth muscle cell differentiation.

Cellular mechanisms controlling smooth muscle cells (SMCs) phenotypic modulation are largely unknown. Intracellular Ca2+ movements are essential to ensure SMC functions; one of the roles of Ca2+ is to regulate calcineurin, which in turn induces nuclear localization of the nuclear factor of activated T-cell (NFAT). In order to investigate, during phenotypic differentiation of SMCs, the effect of calcineurin inhibition on NFAT2 nuclear translocation, we used a culture model of SMC differentiation in serum-free conditions. We show that the treatment of cultured SMC with the calcineurin inhibitor cyclosporine A induced their dedifferentiation while preventing their differentiation. These findings suggest that nuclear translocation of NFAT2 is dependent of calcineurin activity during the in vitro SMC differentiation kinetic and that the nuclear presence of NFAT2 is critical in the acquisition and maintenance of SMC differentiation.

Animals↗

Tumor-inhibitory monoclonal antibodies to the HER-2/Neu receptor induce differentiation of human breast cancer cells.

The HER-2/neu protooncogene (also called erbB-2) encodes a tyrosine kinase receptor for a polypeptide growth-regulatory molecule. Amplification and overexpression of the gene have been frequently observed in human adenocarcinomas and correlated with poor prognosis. To explore the potential of antibody therapy directed at the HER-2/Neu receptor, we have raised a panel of murine monoclonal antibodies to the human protein, and tested their effect on the tumorigenic growth of HER-2/neu-transfected fibroblasts in athymic mice. We previously reported that the i.p. injected antibodies either inhibited or accelerated the tumorigenic growth of HER-2/neu transfectants in athymic mice. Here we report that these opposing effects were induced also by i.v. injected antibodies, they lasted over 7 weeks, and were probably mediated by distinct epitopes on the receptor molecule. To understand the cellular mechanisms underlying antibody-induced tumor inhibition, we tested the effect of the monoclonal antibodies on various cultured human breast cancer cells. Our analysis revealed that the tumor-inhibitory antibodies specifically induced phenotypic cellular differentiation that included growth arrest at late S or early G2 phase of the cell cycle, markedly altered cytoplasm and nuclear morphology, synthesis and secretion of milk components (casein and lipids), and translocation of the HER-2/Neu protein to cytoplasmic and perinuclear sites. The extent of cellular differentiation by various antibodies could be correlated with their tumor-inhibitory potential, whereas a tumor-stimulatory monoclonal antibody or control immunoglobulin were completely inactive with respect to cellular differentiation. Taken together, our in vivo and in vitro studies correlate the tumor inhibitory potential of monoclonal antibodies to HER-2/Neu with their capacity to induce cellular differentiation in vitro. This observation may hold promise for immunotherapy of cancers that express the HER-2/neu oncogene.

Animals↗

Expression of Cx genes in liver and stomach of different embryonic stages.

AIM:To explore the relationship between the rules of Cx gene expression and cellular differentiation in organs of different embryonic stages.METHODS:A series of Cx gene serving as molecular probes and the Northern blot hybrydization were employed to study the Cx gene expression.RESULTS:Cx31,Cx31.1,Cx46 did not express while other Cx genes expressed in the embryonic liver and stomach. The Cx gene expression in the liver and stomach showed different state at different embryonic stages. The Cx gene expression had organic diversity. The expression of Cx26 gene was overlapping in the above organs. Cx43 did not express in the human liver after birth, but it expressed in the embryonic stage.CONCLUSION:The expression state of Cx genes is concordant with cellular differentiation. It might be a key candidate gene to regulate some differentiational events associated with cellular differentiation, proliferation,and morphogenesis in the early embryo.

Journal Article↗

p53 gene mutation spectrum in hepatocellular carcinomas in Hong Kong Chinese.

To examine the significance of mutation of the p53 tumour suppressor gene in the development of human hepatocellular carcinoma in a high-prevalence area for hepatitis B viral infection but a low-exposure area for aflatoxin B1, the spectrum of p53 gene mutations was examined in 21 tumour samples from Hong Kong Chinese patients, all of whom were HBsAg positive. DNA sequencing covering exons 5 to 9 of the p53 gene and Hae III restriction enzyme digestion for preliminary assessment of mutation at codon 249 were performed. Immunohistochemical staining with anti-p53 monoclonal antibodies was done on both tumour and nontumour liver tissues. Six tumours (28.6%) showed a p53 mutation and all were point mutations. Of the six point mutations, two (9.5%) were at codon 249 and both were G to T transversions (AGG-->ATG and AGG-->AGT transversions). The remaining point mutations were transversions scattered at codon 172 (exon 5), 214 (exon 6), 273 (exon 8) and 330 (exon 9). Mutated p53 protein was detected in five of these six cases with demonstrable point mutations by DNA sequencing, in contrast to none detected in all of the 15 cases without demonstrable point mutations. The presence of p53 mutations, including those at codon 249, did not show a significant association with tumour size, sex, age, tumour invasiveness in terms of liver invasion, microsatellites and venous permeation, cirrhosis and encapsulation, but tumours with low cellular differentiation tended to have a higher incidence (71%) of point mutations than those with high cellular differentiation (8%). In conclusion, both the overall p53 mutation rate and that a codon 249 in HCC in Hong Kong Chinese are lower than those reported in tumours from China and sub-Saharan Africa. The low mutation rate at codon 249 is compatible with a low aflatoxin exposure. A special type of p53 mutation has not been found to be associated with hepatitis B viral infection. Mutations of p53 gene tends to occur in tumours with low cellular differentiation, suggesting a late occurrence in the event of tumour progression.

Carcinoma, Hepatocellular↗

Cyclin D1 represses p300 transactivation through a cyclin-dependent kinase-independent mechanism.

Cyclin D1 encodes a regulatory subunit, which with its cyclin-dependent kinase (Cdk)-binding partner forms a holoenzyme that phosphorylates and inactivates the retinoblastoma protein. In addition to its Cdk binding-dependent functions, cyclin D1 regulates cellular differentiation in part by modifying several transcription factors and nuclear receptors. The molecular mechanism through which cyclin D1 regulates the function of transcription factors involved in cellular differentiation remains to be clarified. The histone acetyltransferase protein p300 is a co-integrator required for regulation of multiple transcription factors. Here we show that cyclin D1 physically interacts with p300 and represses p300 transactivation. We demonstrated further that the interaction of the two proteins occurs at the peroxisome proliferator-activated receptor gamma-responsive element of the lipoprotein lipase promoter in the context of the local chromatin structure. We have mapped the domains in p300 and cyclin D1 involved in this interaction. The bromo domain and cysteine- and histidine-rich domains of p300 were required for repression by cyclin D1. Cyclin D1 repression of p300 was independent of the Cdk- and retinoblastoma protein-binding domains of cyclin D1. Cyclin D1 inhibits histone acetyltransferase activity of p300 in vitro. Microarray analysis identified a signature of genes repressed by cyclin D1 and induced by p300 that promotes cellular differentiation and induces cell cycle arrest. Together, our results suggest that cyclin D1 plays an important role in cellular proliferation and differentiation through regulation of p300.

Cyclin D1↗

Identification of a new tumor suppressor gene located at chromosome 8p21.3-22.

Transformation of normal cells into malignant tumor cells, a process termed carcinogenesis, depends on progressive acquisition of genetic alterations. These result in activation of protooncogenes or inactivation of tumor suppressor genes responsible for the loss of proliferative control in tumor cells and the failure to undergo cellular differentiation. The aim of our study was the identification of molecular regulators of carcinogenesis by studying gene expression during induction of cellular differentiation and quiescence in a three-dimensional (3D) cell culture model. Here, we report the discovery of a tumor suppressor gene located at chromosome 8p21.3-22 near marker D8S254. It is ubiquitously expressed in normal tissue and transiently up-regulated during initiation of cellular differentiation and quiescence in 3D cell culture. In contrast, mRNA expression was not detectable in tissue from pancreatic tumor and the pancreatic tumor cell line MIA PaCa-2. Recombinant expression in the tumor cell line MIA PaCa-2 inhibited proliferation, as shown by a 30% reduction of BrdU uptake after recombinant expression. Immunocytochemistry and Western blot analysis of subcellular fractions demonstrated a mitochondrial localization for the mature protein. In conclusion, we identified a tumor suppressor gene at chromosome 8p21.3-22, encoding a mitochondrial protein, controlling cellular proliferation.

Base Sequence↗

Analysis by computer-controlled cell sorter of Friend virus-transformed cells in different stages of differentiation.

In most systems involving cellular differentiation and cellular transformation the biological process is non-synchronous and the sample heterogeneous. In order to answer some of the basic questions about the control mechanisms of cellular changes and the order in which they proceed one must have access to homogeneous classes of cells. Friend virus transformed erythroid cells which are stably maintained in tissue culture can be chemically induced to differentiate and are thus very advantageous for in vitro studies (1-3). With such a system the questions which we pose are a) the reversibility of the differentiation process; b) the order of steps in the production of specialized messenger RNA; c) the time of shut-off of undifferentiated messenger production; d) the relationship of viral RNA production to the differentiation process; e) the onset and extent of specific protein synthesis; f) the correlation of DNA metabolism with the timing or course of events. By using a computer-controlled cell separator we can select live cells on the basis of their macromolecular content, membrane properties (using a new parameter, fluorescence emission anisotropy), and size (4, 5, 34). Thus with proper probes as described here, we are able to select cells at different stages in their differentiation and can begin to attack the questions posed above.

Cell Differentiation↗

Beta-adrenergic receptors of cerebellar astrocytes in culture: intact cells versus membrane preparation.

Experiments were carried out to assess: the influence of culture conditions on the expression of beta-adrenergic receptors in intact glial cells from the central nervous system; and the extent to which quantitation of receptor sites in membrane preparations reflects the receptor population of the whole cells they are derived from. Cerebellar astrocytes were chosen for this study since essentially one receptor subtype, the beta 2 one, is present in adult cerebellum. Intact, attached cerebellar astrocytes exhibit only one class of binding sites for the beta-adrenergic antagonist, [3H]CGP 12177. Replating of the astrocytes after a few days of culture in vitro induces an up-regulation of the receptors. This effect is particularly important when astrocytes are maintained for 6 days in the presence of horse serum, a condition that favors cellular differentiation. Only 30-50% of the beta-adrenergic receptors of the intact cells can be detected on membrane preparations. When membranes are prepared from astrocytes grown either in the presence of horse serum or under chemically controlled medium (i.e. under differentiation promoting conditions) two classes of binding sites for [125I](-)-iodocyanopindolol are revealed. Several hypotheses, mainly related to the morphology of the cells, may provide an explanation for such differences. Studies of the pharmacological specificity of receptors of membrane fractions show that cerebellar astrocytes cultured in vitro exhibit both beta 1 and beta 2 receptor subtypes. The beta 1 subtype receptors are slightly more abundant when astrocytes are grown in fetal calf serum (FCS), a condition under which they exhibit a polygonal, poorly differentiated morphology. When culture conditions favor cellular differentiation, more receptors of the beta 2 subtype are seen, which can be related to what is observed in the adult in vivo where the astrocytes exhibit a differentiated morphology.

Animals↗

Hydrocortisone increases the rate of differentiation of cultured human osteoblasts.

Reduced bone formation is the main finding in glucocorticoid-induced osteoporosis. The aim of this study was to determine whether differentiation of cultured human osteoblasts is inhibited by high concentrations of hydrocortisone. We measured the levels of mRNAs for three markers of cellular differentiation, type 1 collagen (COL1), alkaline phosphatase (ALP), and osteocalcin (OC), in four lines of human osteoblasts from female donors cultured with doses of hydrocortisone from 0 microM to 4 microM. The change in ALP/COL1 mRNA ratio over a given time was used to determine the average rate of differentiation of the cells in a culture. Although basal expression profiles and their changes with time were different for the different cell lines, all cell lines showed a dose-dependent rise in the rate of increase of ALP mRNA relative to COL1 mRNA. However, increase in OC mRNA with time, seen here only in young donor hOBs, was significantly inhibited by 4 microM hydrocortisone, indicating that hydrocortisone can inhibit OC expression while promoting cellular differentiation. The data suggest that increasing concentrations of glucocorticoid, including concentrations similar to plasma levels in patients receiving oral glucocorticoid therapy, increase the rate of cellular differentiation.

Aged↗

Lipopolysaccharide and phorbol 12-myristate 13-acetate both impair monocyte differentiation, relating cellular function to virus susceptibility.

Both lipopolysaccharide (LPS) and phorbol 12-myristate 13-acetate (PMA) impeded monocyte to macrophage differentiation with respect to typical phenotypic modulation and certain phagocyte-related processes. The down-regulation of the porcine monocyte marker SWC1, and up-regulation of the SWC9 macrophage marker were retarded, but not inhibited, as was the differentiation-associated down-regulation of p53 and myeloperoxidase. Despite this clear impairment of macrophage differentiation, not all cellular functions were equally susceptible. Both agents inhibited phagocytosis, but not low-density lipoprotein receptor-associated endocytosis. Only LPS inhibited tartrate-resistant acid phosphatase up-regulation. In contrast, increase of vacuolar acidification rates was more susceptible to PMA. The activity of certain endosomal/lysosomal enzymes - esterase, nucleotidase, peroxidase and cathepsins - was generally enhanced by both LPS and PMA. This contrasted with autophagosomal activity, detected through the induction of an antiviral state. Disruption of autophagosomes and lysosomes (methionine-O-methyl ester), but not lysosomes alone (glycyl-L-phenylalanine) reversed LPS-induced inhibition of virus replication, without influencing the PMA-induced antiviral effect. Thus, PMA is similar to LPS in inhibiting monocyte to macrophage differentiation, when primary blood monocytes are employed, but not all pathways are equally susceptible. The analyses demonstrate that the pathways modulated during monocyte differentiation function somewhat independently. Moreover, certain functions of monocytic cells are more important with respect to the outcome of virus infection, with autophagosomal activities in particular favouring cell survival.

African Swine Fever Virus↗