Intercellular communication between granulosa cells and mouse oocytes: existence and possible nutritional role during oocyte growth.
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The aim of this review is to analyze the different ways by which stem cells and microenvironmental cells may interact. Stem cells are defined as immature cells that ensure the continuous renewal of blood cells. This small set of marrow cells comprises different kinds of cells, differing by their degree of maturity, their commitment, self-renewal ability and repopulating capacity. Microenvironmental cells are fixed marrow cells involved in stem cell survival, proliferation and differentiation. In vivo studies on the distribution within spleen or marrow, of stem cells injected to lethally irradiated mice, have suggested that cells of the microenvironment play a significant role in stem cell proliferation and differentiation. This role has been demonstrated using an in vitro model, i.e. the long-term marrow cultures as described in 1976 by M. Dexter. Analysis of stem cell maintenance in this culture system has made it possible to define the different means by which stromal cells and macrophages (the microenvironmental cells) may control stem cell behavior. Different molecules play a critical role: cytokines (growth factors and inhibitors), adhesion molecules (cell adhesion molecules and molecules belonging to the extracellular matrix) and eventually small peptides. It appears nowadays possible to materially represent the hemopoietic niche, whose existence was postulated by R. Schofield 10 years ago for theoretical reasons related to the the physiology of stem cells.
Mixtures of drug-resistant and drug-sensitive tumour cells growing in 3-dimensional boluses in collagen gel matrix are shown to be effectively coupled so that the response of the mixture is significantly influenced by a subpopulation making up only 1% of the total cells.
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Recent observations have revealed that intercellular connections can be formed through membrane nanotubes. These delicate structures could facilitate transport of organelles and membrane proteins between cells. The sharing of cell surface and cytoplasmic components between cells could be commonplace in biology, but an important physiological role for membrane nanotubes between immune cells is difficult to test with current technology.
Use of cell phones has grown dramatically; however, there remains a gap between people with disabilities and the general public in regard to access to cellular telephony. This article describes the importance of cell phone use among people who use augmentative communication devices. An "off-the-shelf" solution is described and illustrated with the goal of improving access to mobile communication among individuals with significant communication disabilities. Finally, a discussion of the need for universal design of cell phones that includes such features as infrared ports, volume range, speakerphones, matrix displays, EZ buttons, voice dialing, and messaging is presented.
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Findings over the past decades demonstrating persistent neurogenesis in the adult brain have challenged the view of a fixed circuitry in normally functioning brain and raised hopes for self-renewal following brain injury. In addition to providing insights for repair, studying adult neurogenesis may improve our understanding of embryonic development assuming that fundamental mechanisms are similar. It is argued here, using examples of cell:cell communication, that parallels can be drawn between adult and embryonic neurogenesis. Paradoxically, cell:cell communication in neurogenic regions resembles that in a mature neuroglial network. This suggests that differences in the integrative properties of cells and the extracellular matrix molecules may constitute a neurogenic environment or "niche". While reasons for persistent adult neurogenesis in humans remains obscure, recent findings regarding the environmental and activity-driven control of neurogenesis reinforce the original concept of a role for neurogenesis in motor memory formation and refinement of information processing.
The changes in genome conformational state (GCS) induced by low-dose ionizing radiation in E. coli cells were measured by the method of anomalous viscosity time dependence (AVTD) in cellular lysates. Effects of X-rays at doses 0.1 cGy--1 Gy depended on post-irradiation time. Significant relaxation of DNA loops followed by a decrease in AVTD. The time of maximum relaxation was between 5-80 min depending on the dose of irradiation. U-shaped dose response was observed with increase of AVTD in the range of 0.1-4 Gy and decrease in AVTD at higher doses. No such increase in AVTD was seen upon irradiation of cells at the beginning of cell lysis while the AVTD decrease was the same. Significant differences in the effects of X-rays and gamma-rays at the same doses were observed suggesting a strong dependence of low-dose effects on LET. Effects of 0.01 cGy gamma-rays were studied at different cell densities during irradiation. We show that the radiation-induced changes in GCS lasted longer at higher cell density as compared to lower cell density. Only small amount of cells were hit at this dose and the data suggest cell-to-cell communication in response to low-dose ionizing radiation. This prolonged effect was also observed when cells were irradiated at high cell density and diluted to low cell density immediately after irradiation. These data suggest that cell-to-cell communication occur during irradiation or within 3 min post-irradiation. The cell-density dependent response to low-dose ionizing radiation was compared with previously reported data on exposure of E. coli cells to electromagnetic fields of extremely low frequency and extremely high frequency (millimeter waves). The body of our data show that cells can communicate in response to electromagnetic fields and ionizing radiation, presumably by reemission of secondary photons in infrared-submillimeter frequency range.
Endogenous chicken muscle lectin isolated by lactose affinity chromatography inhibits myoblast fusion. Similar lectins isolated from embryonic brain, heart, and liver and from adult intestine exhibit the same ability. Elevated levels of any of these lectins canceled the inhibitory effect. Peanut agglutinin isolated by the same procedure had no effect at any concentration tested. Concanavalin A affected fusion only at high concentrations. Muscle lectin was shown to agglutinate myoblasts in microtiter plates, whereas exogenous addition in culture inhibited alignment as seen by time lapse microcinematography. Cell-to-cell communication between lectin-treated cells was shown by nucleotide exchange, and lectin-coated culture dishes did not affect cell attachment. Our evidence shows a lack of specificity to muscle, but suggests an aggregating capacity between cells, or possibly an interaction between the cell membrane and the extracellular matrix.
Using an in vitro assay system to measure a form of cell-cell communication in Chinese hamster V79 cells, several purified polybrominated biphenyl (PBB) congeners were analyzed for their ability to affect colony-forming ability and "metabolic cooperation" in these cells. Results clearly demonstrate the assay's ability to distinguish differences in the cytotoxic and metabolic cooperation-inhibiting properties of these congeners related to their structure. It appears that if a carbon ortho to the bridge carbon of each phenyl ring is brominated, the molecule has the property by which metabolic cooperation is inhibited. The results suggest that several PBB congeners share at least one property associated with several known tumor promoters, such as the phorbol esters. Although we have not ruled out that the mixture of PBB congeners might contain initiators or that various PBB metabolites would be mutagen/initiators, based on these and other results, it was concluded that the reported carcinogenic potential of PBB seems to be mediated by its action as a tumor promoter, rather than as a complete carcinogen or an initiator.
Monocytes/macrophages and synovial fibroblast-like cells are in intimate contact in the synovium and are believed to play a critical role in the development of rheumatoid arthritis. We investigated the effects of monocyte-synoviocyte interactions in vitro on cytokine release and the expression of adhesion molecules. Using a sensitive Western blot assay, we found that VCAM-1 and ICAM-1 expression were up-regulated in synoviocytes following coculture. The interaction also resulted in the accumulation of TNF and IL-6, but not IFN-gamma in the culture medium. Culture supernatant from monocyte-synoviocyte samples effectively induced adhesion molecules in synoviocytes. Anti-TNF partially inhibited the increase in VCAM-1 and ICAM-1 expression, indicating that TNF in part mediates VCAM-1 and ICAM-1 expression. Interestingly, the induction of cytokines and adhesion molecules did not require cell contact between monocytes and synoviocytes, suggesting cell communication via soluble factors. T cell cytokines enhanced the induction of adhesion molecules induced by the monocyte-synoviocyte interaction. IFN-gamma and IL-4, which are produced by distinct T helper subsets, had differential effects on monocyte-synoviocyte interactions. IFN-gamma had a minimal effect on VCAM-1 expression by synovial fibroblasts, but synergized with monocytes to dramatically up-regulate ICAM-1 expression. IL-4 had no effect on ICAM-1 expression but enhanced monocyte-induced expression of VCAM-1. Our results demonstrate that the up-regulation of adhesion molecules following monocyte-synoviocyte interactions is mediated by soluble factors and can be regulated by specific T cell cytokines.
An original system was developed to detect intercellular communication between epithelial cells of rat colon mucosa. Cell-to-cell communication was tested both in normal and in azoxymethane (AOM)-induced aberrant crypts in an attempt to identify chemically-induced modifications of cell properties. Stripes of unstained live tissue were superfused and oxygenated at room temperature and single cells at the top of the crypt were injected with fluorescent dyes. The bottom cells were filled in isolated crypts. Dyes injected into cells at the surface of the mucosa failed to diffuse to adjacent ones, whereas cells at the base of the crypts were dye-coupled. Surface cells from aberrant crypt foci (ACF) did not transfer the dye, therefore behaving like normal crypts. These results indicate that the pattern of intercellular communication between colon crypt cells changes as these cells differentiate and migrate to the top of the crypts and that the pattern of dye transfer between surface cells is maintained in ACF.
Communication within the hematopoietic-neuroendocrine-immune axis is partly mediated by neurotransmitters (e.g. substance P, SP) and cytokines. SP mediates neuromodulation partly through the stimulation of bone marrow (BM) progenitors. This study shows that SP, through the neurokinin-1 receptor, stimulates the proliferation of primitive hematopoietic progenitors: cobblestone-forming cells (CAFC, CD34+). This effect is optimal when macrophage is included within the fibroblast support. Indirect induction of IL-1 could be important in the proliferation of CAFC colonies by SP. Phenotypic and functional studies suggest that SP might directly interact with the CD34+/CD45(dim) population. These studies indicate that SP can initiate a cascade of biological responses in the BM stroma and stem cells to stimulate hematopoiesis.
Cell to cell communication via gap junctions is essential in the maintenance of the homeostatic balance of multicellular organisms. Aberrant intercellular gap junctional communication (GJIC) has been implicated in tumor promotion, neuropathy and teratogenesis. Oxidative stress has also been implicated in similar pathologies such as cancer. We report a potential link between oxidative stress and GJIC. Hydrogen peroxide, a known tumor promoter, inhibited GJIC in WB-F344 rat liver epithelial cells with an I50 value of 200 microM. Inhibition of GJIC by H2O2 was reversible as indicated by the complete recovery of GJIC with the removal of H2O2 via a change of fresh media. Free radical scavengers, such as t-butyl alcohol, propylgallate, and Trolox, did not prevent the inhibition of GJIC by H2O2, which indicated that the effects of H2O2 on GJIC was probably not a consequence of aqueous free radical damage. The depletion of intracellular GSH reversed the inhibitory effect of H2O2 on GJIC. The treatment of glutathione-sufficient cells with H2O2 resulted in the hyperphosphorylation of connexin43, which is the basic subunit of the hexameric gap junction protein, as determined by Western blot analysis. TPA, a well-known tumor promoter, also inhibits GJIC via hyperphosphorylation of GJIC, which is a result of protein kinase-C activation. However, H2O2 also induced hyperphosphorylation in GSH-deficient cells that had normal rates of GJIC. Therefore, the mechanism of GJIC inhibition must be different from the TPA-pathway and involves GSH.
To analyze the possible mechanisms by which coxsackie B1 virus infection affects the invasiveness of Shigella flexneri, we have studied the influence of intracellular levels of Na+ and K+, ATPase activity, cytoplasmic membrane potential, cAMP level and cell communication through gap junctions. 3h after adsorption of viable or UV-inactivated coxsackie B1 virus the Na(+)-K+ gradient of the cell collapsed, ATPase activity decreased, the cytoplasmic membranic potential-dependent tetraphosphonium ion uptake were reduced. No changes in cAMP or intercellular cell communication were observed. S. flexneri invasiveness in HEp-2 cell pretreated with viable or UV-inactivated coxsackie B 1 virus was enhanced, but bacterial invasiveness was unchanged in K(+)-depleted HEp-2 cells, cell cultures with high intracellular Na+ content or ouabain pre-treated cells compared to control cells. We found no correlation between the enhanced bacterial invasiveness in the early phase of coxsackie B 1 virus infection in HEp-2 cell cultures and intracellular K+ depletion, high intracellular Na+ content, inhibited Na(+)-K+ ATPase activity or membranic depolarization.
Communication between exon boundaries is a central feature of the exon definition model of pre-mRNA splice-site selection and an exon-bridging interaction involving U1 small nuclear RNA (snRNA) paired with the 5' splice site (5'ss) has been identified previously. It has become increasingly clear, however, that the 5'ss is not defined relative to the base-pairing interaction with U1, suggesting that a connection in the proposed line of communication between exon boundaries is missing. To explore this issue, we have first sought to characterize the role in mammalian 5'ss selection of a previously suggested base-pairing interaction with U6 snRNA. Using transfection experiments, we show that mutations at positions 5 and 6 of a 5'ss associated with an internal exon can be suppressed by compensatory changes in the first two positions of a conserved hexanucleotide of U6 RNA. The specificity of the effect was established by covariation experiments as well as by experiments with two splice sites arranged in tandem. Suppression of 5'ss mutations by U6 was more efficient when U1 could pair nearby than when pairing was restored further away and individual U1 RNAs stimulated U6-defined proximal sites more efficiently than distal sites. These results are interpreted to suggest that U1 acts to direct 5'ss choice by U6 to matching sequences nearby. Our work supports a central role for base-pairing with U6 snRNA in mammalian 5'ss selection and suggests how the interaction may be established properly despite the limited complementarity involved.