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At least 775 records · Page 43Linked to original sources
PubMed1989

Patterning during pupal commitment of the epidermis in the butterfly, Precis coenia: the role of intercellular communication.

The commitment of cells to pupal development in the larvae of holometabolous insects can be prevented by treatment with juvenile hormone (JH) or a JH mimic during a critical period early in the last larval instar. By treating larvae of different ages with a JH mimic, pupal commitment of the epidermis of the butterfly, Precis coenia, was found to occur in a strict temporal and spatial progression, which was serially homologous and occurred independently in each segment. The mechanism underlying this sequence of pupal commitment was examined by cauterizing regions of the epidermis to observe the effects of local ablation on the pattern of pupal commitment revealed by treatment with the JH mimic. Cautery of the segmental site of origin of pupal commitment, the dorsal midline, suppressed pupal commitment in the rest of the operated segment, indicating that the midline has a special effect on commitment of the rest of the segment. Cautery off the midline produced asymmetries in the pattern of pupal commitment; when placed close to the midline, such cauteries prevented pupal commitment in the region "downstream" of the cautery, suggesting that a signal (diffusible or transducible) emanates from the midline. Finally, cautery of a circle around the midline inhibited pupal commitment only outside the circle, showing that cautery could act as a barrier to the passage of a signal coming from the midline. These results suggest that inductive as well as hormonal signals are involved in the regulation of pupal commitment in the epidermis of the lepidopteran, P. coenia.

Animals↗
PubMed1984

Monoclonal antibody ECCD-1 inhibits intercellular communication in teratocarcinoma PCC3 cells.

The monoclonal antibody ECCD-1 recognizing a certain class of cell surface proteins inhibits the Ca2+-dependent cell-to-cell adhesion in teratocarcinoma stem cells. In this paper, we studied the effect of ECCD-1 on cell-to-cell communication in PCC3 cells by measuring the transfer of lucifer yellow between cells. To this aim, PCC3 cells were cultured in the presence of ECCD-1 for various periods, and then the fluorescent dye was injected into a cell located in the center of cell colonies, followed by counting number of cells to which the dye was transferred. The results showed that ECCD-1 inhibits the dye transfer between cells, suggesting that the Ca2+-dependent cell-to-cell adhesion system (CDS) is essential for the functions of gap junction.

Animals↗
PubMed1988

Induction of intercellular communications in epithelial cell cultures.

A popular criterion of cell-cell communication in tissue cultures is dye coupling: the ability of the injected fluorescent dye of low molecular weight to be transferred from one cell to another. We report about a new factor which induces cell-to-cell dye coupling in previously uncoupled epithelial sheets. Paradoxically it is the standard fluorescent microscopy itself (that is, blue light of 320- to 480-nm wavelength) which induces rapid morphological alterations of cell culture followed by the transfer of fluorescent dye from one cell to another. Thus monitoring cell-cell dye coupling by fluorescent microscopy may itself induce the dye coupling in previously uncoupled epithelial cells.

Animals↗
PubMed1986

Hormones, neurosecretions, and growth factors as signal molecules for intercellular communication.

Chemical signals, whether in the form of hormones, neurosecretions (neurotransmitters and neuropeptides), or growth factors and chalones are used to communicate information to cells at all stages of their life cycle. These signals inform the cells when it is time to progress through developmental change, when to change the rates of various activities (e.g. metabolism or contraction), and, in some cases, even when it is time to die. Throughout all of these interactive exchanges, the signal molecule itself carries no intrinsic message of a universal nature. The chemical identity of the signal molecule has meaning only for those cells competent to receive the signal (i.e. does it possess an appropriate receptor?). Moreover, it is the nature of the cell receiving the signal (itself the product of innumerable previous encounters with signals from other cells) that dictates the specific response that a particular signal will evoke. The signal emitted by the communicating cell only informs the target cell that it is time to act in a manner consistent with that signal. The majority of the discussion has been from the perspective of vertebrate organisms. Moreover, of necessity, the discussion has been general and superficial. The primary objective of the preceding discussion has been to underscore major similarities and differences existing among hormones, neurosecretions (neurotransmitters and neuropeptides), and growth factors as information-bearing substances used in communication among vertebrate cells. It should be realized that similar means of communication are employed by multicellular invertebrates, by plants, and even by single-celled organisms such as the protists and bacteria.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Communication↗
PubMed1986

Intercellular communication mediated by VIP in the cerebral cortex.

A growing number of biologically active peptides is being identified within the central nervous system (CNS). According to currently accepted criteria, several of these peptides, including VIP, can be viewed as neurotransmitters. Recent immunohistochemical and pharmacological investigations have been directed at the characterization of the position of VIP neurons in the circuitry of the cerebral cortex. From these studies some views on the possible function of VIP neurons in this CNS region are beginning to emerge. In the cerebral cortex, VIP neurons constitute a rather homogeneous population of intracortical, bipolar and radially oriented cells, which arborize locally, within cortical columns of 60-100 micron diameter. The cellular actions of VIP in the cerebral cortex include the stimulation of cAMP formation and of glycogen breakdown. A certain degree of cellular resolution of these two actions of VIP has been achieved by using purified preparations. Thus VIP stimulates cAMP formation in cerebral microvessels and in cultured astrocytes; in this latter cell type VIP also promotes glycogenolysis. Furthermore, VIP interacts synergistically with norepinephrine to stimulate cAMP formation and to inhibit the firing rate of spontaneously active identified cortical neurons. VIP neurons appear therefore to be strategically positioned to regulate the coupling between energy metabolism, blood flow and neuronal activity with great spatial selectivity and at a fine level of cortical resolution.

Animals↗
PubMed1992

Evolution of regulation of steroid-mediated intercellular communication in vertebrates: insights from flavonoids, signals that mediate plant-rhizobia symbiosis.

Various flavonoids, such as genistein, luteolin, and coumestrol, have actions in mammals that are mediated by binding either to classical estrogen receptors or to type II receptors, which also bind estrogen. These actions are of intense interest because they may be the basis for the protective actions of plants against certain cancers, such as breast cancer. The biological activity of flavonoids in mammals raises some questions. Is the hormonal action of flavonoids "an accident" derived from their phenolic groups and general hydrophobicity, which gives them some properties in common with estrogens? Or do flavonoids regulate gene transcription in other organisms? And, if so, is there a connection between their actions in these organisms and in mammals? Some answers to these questions are provided by the actions of plant-derived flavonoids in regulating gene transcription in rhizobia, bacteria that form nitrogen-fixing nodules in the roots of legumes, which has several interesting similarities with steroid-mediated actions in vertebrates. First, there is specificity in the actions of flavonoids in rhizobia; oxidation or reduction of the flavonoid or removal of a hydroxyl group can alter its biological activity. Moreover, some flavonoids are anti-inducers functioning like steroid antagonists to negate the actions of inducers. Also there are sequence similarities between various steroid metabolizing enzymes and proteins found in rhizobia, which indicates that these proteins are derived from a common ancestor. For example, 17 beta-hydroxysteroid dehydrogenase, which catalyzes the interconversion of the alcohol and ketone a C17 on estrogens and androgens, 11 beta-hydroxysteroid dehydrogenase, which catalyzes the interconversion of the alcohol and ketone at C11 of glucocorticoids, and 3 alpha,20 beta-hydroxysteroid dehydrogenase, which catalyzes the interconversion of the alcohol and ketone at C20 of corticosteroids, are homologs of proteins found in rhizobia. Thus, the binding of flavonoids to vertebrate proteins may represent an evolutionary linkage between the actions of steroids in mammals and communication between plants and rhizobia.

Animals↗
PubMed2005

[Gap junction-mediated intercellular communication in astrocytes and neuroprotection].

Neuroglial interaction represents a concept that is now more and more integrated in the attempts to understand who does what and how in neuronal processing and survival, in normal as well as in pathological situations. The purpose of the review is to provide an overlook about the role of glial cells, mainly astrocytes, in neuroprotection. Since a typical feature of glia is to be connected by gap junctions that allow them to be organized as a communicating network(s), we will focus this review on what is known about the contribution of astrocyte gap junctions (AGJ) in neuronal survival. As neuroglial interaction and AGJ are both affected during neurodegenerative diseases, we will also consider the above mentioned glial properties in a pathological context with a special interest in Alzheimer's disease.

Alzheimer Disease↗
PubMed2005

The extracellular zinc-sensing receptor mediates intercellular communication by inducing ATP release.

Taste and salivary secretion disorders have been linked to zinc deficiency, indeed zinc is found in secretory granules in the salivary gland. The signaling role for the zinc release in this tissue, however, is poorly understood. Here, we address the signaling pathways and physiological role of the zinc-sensing receptor, ZnR, in the ductal salivary gland cell line, HSY. Exposure of these cells to zinc triggered intracellular Ca2+ release from thapsigargin-sensitive stores. The G alpha q inhibitor, YM-254890 (1 microM), eliminated the Zn2+-dependent Ca2+ response, demonstrating that ZnR is a G alpha q-coupled receptor. Dose-response curves yielded an apparent K0.5 of 36 microM and a Hill coefficient of 7 in the absence of extracellular Ca2+, and K0.5 of 55 microM with a Hill coefficient of 3 in its presence. This indicates that although Zn2+ is essential for ZnR activation, Ca2+ may affect the receptor co-operativity. The homologous desensitization pattern of ZnR was characterized by pre-exposure of cells to Zn2+ at concentrations found to activate the receptor. Re-exposure of cells to Zn2+ elicited an attenuated Zn2+-dependent Ca2+ response for at least 3 h, indicating that the ZnR is strongly desensitized by Zn2+. Finally, we studied the paracrine affects of ZnR using a co-culture consisting of the HSY cells and vascular smooth muscle cells (VSMCs). While no Zn2+-dependent Ca2+ release was observed in VSMC alone, application of Zn2+ to the co-culture induced a Ca2+ rise in both HSY cells and VSMC. This Ca2+ rise was inhibited by the ATP scavenger, apyrase. Taken together, our results demonstrate that ZnR activity is monitored in salivary cells and is modulated by extracellular Ca2+. We further show that ZnR enhances secretion of ATP, thereby linking zinc to key signaling pathways involved in modification of salivary secretions by the ductal cells.

Adenosine Triphosphate↗