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Results for “intercellular communication”

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At least 865 records · Page 48Linked to original sources
PubMed1995

A proteinous factor mediating intercellular communication during the transition of Dictyostelium cells from growth to differentiation.

In general, cell differentiation and proliferation are mutually exclusive. Transition of the cellular slime mold Dictyostelium discoideum from growth to differentiation is triggered mainly by a secreted factor(s) in addition to nutritional deprivation. To purify and identify the factor required for the growth/differentiation transition, a new assay system was designed. Under low-nutrient conditions, cells could grow to multiply, but never developed. The cellular development including aggregation, however, was induced by the addition of conditioned medium (CM) in which growing or starving Dictyostelium cells had been cultured. The CM inhibited the synthesis of nuclear DNA and induced the cells to acquire chemotactic competence to cAMP, thus suggesting the presence of a secreted factor(s) required for growth/differentiation transition in the CM. The active factor(s) in CM (referred to as CMF450; conditioned medium factor) was found to be sensitive to heat and have a large molecular size. The CMF450 was purified using FPLC through a gel filtration column, and was identified to be a proteinous macromolecule of Mr 450 kDa, which was mainly composed of 94 kDa, 79 kDa, and 49 kDa subunits under a native condition.

Amino Acid Sequence↗
PubMed1999

In vivo induction of pyrimidine dimers in human skin by UVA radiation: initiation of cell damage and/or intercellular communication?

Pyrimidine dimers participate as important factors in ultraviolet-induced lethality, mutagenicity and tumorgenicity. Substantial efforts have been made in recent years to understand the induction of pyrimidine photodimers and their repair in human skin cells exposed to low physiological fluences of UV-light. Dimers are known to be efficiently induced after UVC and UVB irradiation, but these photoproducts are also highly induced in DNA isolated from human skin irradiated with UVA. By using a sensitive immunohistochemistry dimer detection assay, we confirm that in vivo UVA radiation induces substantial amounts of these DNA changes in the epidermis; in addition, this technique detects them far into the reticular dermis. A considerable number of these photodimers were also seen in non-irradiated control skin up to two centimeters from the irradiation site. All the lesions persist for at least two days post-irradiation. These results sustain the hypothesis that pyrimidine dimer formation and excision could be a modality of epidermal communication.

Adult↗
PubMed2006

Blood-neural barrier: intercellular communication at glio-vascular interface.

The blood-neural barrier (BNB), including blood-brain barrier (BBB) and blood-retinal barrier (BRB), is an endothelial barrier constructed by an extensive network of endothelial cells, astrocytes and neurons to form functional "neurovascular units", which has an important role in maintaining a precisely regulated microenvironment for reliable neuronal activity. Although failure of the BNB may be a precipitating event or a consequence, the breakdown of BNB is closely related with the development and progression of CNS diseases. Therefore, BNB is most essential in the regulation of microenvironment of the CNS. The BNB is a selective diffusion barrier characterized by tight junctions between endothelial cells, lack of fenestrations, and specific BNB transporters. The BNB have been shown to be astrocyte dependent, for it is formed by the CNS capillary endothelial cells, surrounded by astrocytic end-foot processes. Given the anatomical associations with endothelial cells, it could be supposed that astrocytes play a role in the development, maintenance, and breakdown of the BNB. Therefore, astrocytes-endothelial cells interaction influences the BNB in both physiological and pathological conditions. If we better understand mutual interactions between astrocytes and endothelial cells, in the near future, we could provide a critical solution to the BNB problems and create new opportunities for future success of treating CNS diseases. Here, we focused astrocyte-endothelial cell interaction in the formation and function of the BNB.

Animals↗
PubMed1998

[Cytokines: soluble factors in intercellular communication].

Cytokines (cyto:cell; kine:factor) are produced by cells and serve as chemical messengers for one type of intracellular communication. Cytokines play a central role in host defense mechanisms. Defense against infectious and tumoral disease depends on nonspecific myelomonocyte defenses in conjunction with specific immune processes. Both systems are regulated by various leukocytes in the blood and tissue. All these cell components are produced in the bone marrow from hematopoietic stem cells. Cytokines are soluble messengers allowing deployment and coordination of all cell systems. Despite the complexity of the cytokine network, we now have a better understanding of the interactions between the different components determining secretion and activity of these mediators. This knowledge may hold the promise of better control of immune and inflammatory responses. Experimental data shows that the cytokine balance can be modulated in auto-immune, immune deficiency, and malignant diseases, opening up new perspectives for therapy and perhaps vaccination.

Cell Communication↗
PubMedDate not supplied

Effects of Aroclor 1254 on intercellular communication in human keratinocytes.

It has been previously described that Aroclor 1254 can inhibit GJIC in rodent liver cells where it is known to be a tumor promoter, while the possibility that Aroclor 1254 exerts its inhibitory effects on GJIC in human keratinocytes and acts as a human skin tumor promoter, deserves further attention. In the present study the effects of Aroclor 1254 were examined on gap junction channel permeability, on connexin 43 (Cx 43) expression at mRNA and protein level and on ultrastructural modification to add further experimental evidence to its inhibitory effect on GJIC. The results were compared to those induced by 12-O-tetradecanoylphorbol-13 acetate (TPA), a tumor promoter known to be a potent inhibitor of GJIC in human skin cells and to those induced by benzo[a]pyrene (B[a]P) known for its genotoxic activity. Our data show increased Cx 43 protein expression in Aroclor 1254 and TPA-treated cultures compared to controls, decreased Cx 43 protein level in those exposed to B[a]P, while Cx 43 gene expression (Cx 43 mRNA) was unaffected by the treatments. In Aroclor and TPA-treated keratinocytes, the ultrastructural examination showed residues of junctional systems expressed by specular, short tracts of the faced plasma membranes. In contrast, the contacts between plasma membranes of adjacent B[a]P treated keratinocytes were more extended. A clear inhibition of gap junction channel permeability due to Aroclor 1254 and TPA was also manifest by Lucifer yellow dye test compared to B[a]P-treated cultures where dye spreading to the neighbouring cells and to the extracellular space occurred. The present data, in addition to confirming inhibition of GJIC mediated by Aroclor 1254 in human keratinocytes, which were found to be comparable to those induced by TPA, suggest that GJIC inhibition is associated with increased Cx 43 protein expression without significant modification of its gene expression.

Analysis of Variance↗
PubMed2001

Breast cancer metastatic potential correlates with a breakdown in homospecific and heterospecific gap junctional intercellular communication.

Breast cancer progresses toward increasingly malignant behavior in tumorigenic and metastatic stages. In the series of events in the metastatic stage, tumor cells leave the primary tumor in breast and travel to distant sites where they establish secondary tumors, or metastases. In this report, we demonstrate that cell-cell communication via gap junctions is restored in the metastatic human breast carcinoma cell line MDA-MB-435 when it is transfected with breast metastasis suppressor 1 (BRMS1) cDNA. Furthermore, the expression profile of connexins (Cxs), the protein subunits of gap junctions, changes. Specifically, the expression of BRMS1 in MDA-MB-435 cells increases Cx43 expression and reduces Cx32 expression, resulting in a gap junction phenotype more similar to normal breast tissue. Taken together, these results suggest that gap junctional communication and the Cx expression profile may contribute to the metastatic potential of these breast cancer cells.

Breast Neoplasms↗
PubMed2004

Intercellular communications induced by random fluctuations.

This paper investigates a general coupled noisy system for a cell-cell communication in a multi-cell system. The main conclusion is that appropriate noise intensity and coupling strength are capable of driving the coupled system to synchrony, which may be exploited by biological organisms to actively facilitate mutual communication. A multi-cell system with a synthetic gene network with both noises and delays is adopted to demonstrate the effect of noises on cellular communication.

Adaptation, Physiological↗
PubMedDate not supplied

[Export of metabolites by the proteins of the DMT and RhtB families and its possible role in intercellular communication].

The earlier published and new experimental data are summarized on the properties of the genes encoding the membrane proteins of the DMT family (RhtA (YbiF), EamA (YdeD), YijE, YddG, YedA, PecM, eukaryotic nucleoside phosphate sugar and hexose phosphate transporters), the RhtB/LysE family (RhtB, RhtC, LeuE, YahN, EamB (YfiK), ArgO (YggA), CmaU), as well as some other families (YicM, YdhC, YdeAB, YdhE (NorE)). These proteins are involved in the export of amino acids, purines, and other metabolites from the cell. The expression of most of the genes encoding these proteins is not induced by the substrates they transport but is controlled by the global regulation systems, such as the Lrp protein, and activated by the signal compounds involved in the intracellular communication. The level of expression, assessed in experiments on translational fusion of the corresponding bacterial genes with the beta-galactosidase gene, depends on the growth phase of the bacterial culture, composition of the medium, and some stress factors, such as pH osmolarity or decreased aeration. The efflux of normal cell metabolites is assumed to be the natural function of these proteins. This function may play a role in density-dependent behavior of cell populations (quorum sensing). It may have been enhanced in the course of evolution via specialization of these proteins in the efflux of compounds derived from metabolic intermediates and adjusted to the role of transmitters.

Amino Acids↗
PubMed1991

Membrane-anchored forms of EGF stimulate focus formation and intercellular communication.

Epidermal growth factor (EGF) is the prototype for a small family of soluble proteins that bind to and activate the EGF receptor. These proteins are derived from larger propeptides that are anchored to the plasma membrane. Although the signalling properties of soluble EGF are well-characterized, the signalling potential of the membrane-anchored form had not been determined. We therefore investigated whether membrane-anchored EGF can stimulate the EGF receptor. An EGF mini-gene expression system that we had previously constructed for expression of soluble EGF was modified to encode anchored forms of EGF. In the encoded proteins EGF was fused to the spacer in the EGF propeptide that separates EGF from the transmembrane domain. The spacer was followed by vesicular stomatitis virus G protein transmembrane and cytoplasmic domain sequences. Three forms of EGF/G fusion protein were expressed in rat fibroblasts. The plasmids for expression of anchored EGF induced focus formation in rat fibroblasts, indicating that anchored EGF can cause autocrine transformation. When mixed with indicator HeLa cells, cell lines expressing EGF/G fusion proteins activated the HeLa EGF receptor. This activation was mediated by cell-associated, rather than soluble EGF. The finding that membrane-anchored EGF is capable of activating the EGF receptor on neighboring cells has broad implications for the functions of EGF in the organism.

Animals↗
PubMed1989

Junctional intercellular communication is cooperatively inhibited by oncogenes in transformation.

We examined the actions of the cellular src (c-src) and adenovirus E1A genes on junctional cell-to-cell communication. Neither gene causes complete transformation of NIH3T3 cells on its own, but the two do so in conjunction with one another. This cooperation goes hand in hand with summation of the actions of the two genes on junctional communication: junctional permeability is reduced when the cells are transfected with either gene; it is reduced significantly more when they are transfected with both. This cooperative loss of communication approaches the noncooperative loss induced by the viral src gene (v-src), chimeric c-src/v-src, or Tyr527-mutant c-src--genes that cause transformation on their own. This provides a rationale for the hitherto unexplained complementation of the two oncogenes in carcinogenesis; it is the expected behavior if the loss of communication is causal in the decontrol of growth in transformation.

Adenovirus Early Proteins↗
PubMed1988

[Histologic study of the outcome of components of nerves of human corpses grafted in nude mice (a model of chimeric intercellular communication)].

Human corpse nerves are microsurgically grafted in nude mouse and biopsied from 1 to 152 days after graft. Schwann cells ever survived and probably produce angiogenic factors stimulating mice vessels. Others nerves are grafted end to end with mouse sciatic nerve. Mouse's neurites invading grafts are surrounded by human Schwann cells and set up normal chimeric nerve.

Adult↗