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At least 739 records · Page 41Linked to original sources
PubMed2005

Polarized uterine epithelial cells preferentially present antigen at the basolateral surface: role of stromal cells in regulating class II-mediated epithelial cell antigen presentation.

To study Ag presentation in the female reproductive tract, DO11.10 TCR transgenic mice specific for the class II MHC-restricted OVA(323-339) peptide and non-transgenic BALB/c mice were used. We report here that freshly isolated uterine epithelial cells, uterine stromal, and vaginal APCs present OVA and OVA(323-339) peptide to naive- and memory T cells, which is reduced when cells are incubated with Abs to CD80 and 86. To determine whether polarized primary epithelial cells present Ags, uterine epithelial cells were cultured on cell inserts in either the upright or inverted position. After reaching confluence, as indicated by high transepithelial resistance (>2000 ohms/well), Ag presentation by epithelial cells incubated with memory T cells and OVA(323-339) peptide placed on the basolateral surface (inverted) was 2- to 3-fold greater than that seen with epithelial cells in contact with T cells and peptide on the apical surface (upright). In contrast, whereas freshly isolated epithelial cells process OVA, polarized epithelial cells did not. When epithelial cells grown upright on inserts were incubated with T cells and OVA(323-339) peptide, coculture with either hepatocyte growth factor or conditioned stromal medium increased epithelial cell Ag presentation (approximately 90% higher than controls). These studies indicate that uterine stromal cells produce a soluble factor(s) in addition to a hepatocyte growth factor, which regulates epithelial cell Ag presentation. Overall, these results demonstrate that polarized epithelial cells are able to present Ags and suggest that uterine stromal cells communicate with epithelial cells via a soluble factor(s) to regulate Ag presentation in the uterus.

Animals↗
PubMed2001

Gene expression in atherogenesis.

It is conceivable that the extent and spatio-temperal expression of dozens or even a few hundred genes are significantly altered during the development and progression of atherosclerosis as compared to normal circumstances. Differential gene expression in vascular cells and in blood cells, due to gene-gene and gene-environment interactions can be considered the molecular basis for this disease. To comprehend the coherence of the complex genetic response to systemic and local atherosclerotic challenges, one needs accessible high through-put technologies to analyze a panel of differentially expressed genes and to describe the interactions between and among their gene products. Fortunately, new technologies have been developed which allow a complete inventory of differential gene expression, i.e. DD/RT-PCR, SAGE and DNA micro-array. The initial data on the application of these technologies in cardiovascular research are now being reported. This review summarizes a number of key observations. Special attention is paid to a few central transcription factors which are differentially expressed in endothelial cells, smooth muscle cells or monocytes/ macrophages. Recent data on the role of nuclear factor-kappaB (NF-kappaB) and peroxisome proliferation-activating receptors (PPARs) are discussed. Like the PPARs, the NGFI-B subfamily of orphan receptors (TR3, MINOR and NOT) also belongs to the steroid/thryroid hormone receptor superfamily of transcription factors. We report that this subfamily is specifically induced in a sub-population of neointimal smooth muscle cells. Furthermore, intriguing new data implicating the Sp/XKLF family of transcription factors in cell-cell communication and maintenance of the atherogenic phenotype are mentioned. A member of the Sp/XKLF family, the shear stress-regulated lung Krüppel-like factor (LKLF) is speculated to be instrumental for the communication between endothelial cells and smooth muscle cells. Taken together, the expectation is that the fundamental knowledge obtained on atherogenesis and the data that will be acquired during the coming decade with the new, powerful high through-put methodologies will lead to novel modalities to treat patients suffering from cardiovascular disease. In view of the phenotypic changes of vascular and blood-borne cells during atherogenesis, therapeutic interventions likely will focus on reversal of an acquired phenotype by gene therapy approach or by using specific drugs which interfere with aberrant gene expression.

Animals↗
PubMed2001

The role of hypo-osmotic swelling test in recurrent abortions.

The role of male factors in abortions has not been studied extensively. We undertook this study to determine if there was any relationship between hypo-osmotic swelling test score and recurrent abortions. This was a cross-sectional case control study conducted at the semen analysis laboratory at a tertiary level referral centre. The male partners of 25 patients who had three or more first trimester abortions of unknown etiology were chosen as cases. Controls were 26 unmarried volunteers with unknown fertility potential to represent the entire population. The conventional seminal parameters were studied according to WHO guidelines. The HOS test score were obtained by the method advocated by Jayendran et al. There were no statistically significant differences in mean sperm count, percentage motility and morphology among the cases and controls. We found a low hypo-osmotic swelling test score among the cases [55.7 +/- 1.197 (SEM)] than the controls [69.3 +/- 1.143 (SEM)] which was statistically significant [P < 0.001]. The normal spermatozoal membrane is the prerequisite for the specialized cell-to-cell communications and cell-to-cell binding. In spite of apparently normal semen analysis, subtle membrane defects in the spermatozoa, which could be the cause of defective membrane functions in the embryo effecting miscarriages, can be elucidated by the hypo-osmotic swelling test.

Abortion, Habitual↗
PubMed2002

Expression and physiological actions of cholecystokinin in rat taste receptor cells.

Gustatory perception arises not only from intracellular transduction cascades within taste receptor cells but also from cell-to-cell communication among the cells of the taste bud. This study presents novel data demonstrating that the brain-gut peptide cholecystokinin (CCK) is expressed in subsets of taste receptor cells, and that it may play a signaling role unknown previously within the taste bud. Immunocytochemistry revealed positively stained subsets of cells within taste buds throughout the oral cavity. These cells typically displayed round nuclei with full processes, similar to those classified as light cells. Peptide expression was verified using nested PCR on template cDNA derived from mRNA extracted from isolated posterior taste buds. Multiple physiological actions of cholecystokinin on taste receptor cells were observed. An outward potassium current, recorded with the patch-clamp technique, was inhibited by exogenous application of sulfated cholecystokinin octapeptide in a reversible and concentration-dependent manner. Pharmacological analysis suggests that this inhibition is mediated by CCK-A receptors and involves PKC phosphorylation. An inwardly rectifying potassium current, typically invariant to stimulation, was also inhibited by cholecystokinin. Additionally, exogenous cholecystokinin was effective in elevating intracellular calcium as measured by ratiometric techniques with the calcium-sensitive dye fura-2. Pharmacology similarly demonstrated that these calcium elevations were mediated by CCK-A receptors and were dependent on intracellular calcium stores. Collectively, these observations suggest a newly discovered role for peptide neuromodulation in the peripheral processing of taste information.

Animals↗
PubMed2003

[Studies on the testis regression related gene profile in aged male].

OBJECTIVE: To understand the mechanism of testis regression in aging male. METHODS: Human testis tissues were obtained during related operation with informed consent (normal young male 3 cases and aged male 3 cases). Total RNA was isolated by QIAGEN RNAeasy kit. Differentiations of gene expression were studied by Clon-Tech cDNA microarray methods and the differential expression gene in aged male were classified by Venter's classify system and the candidate genes were investigated by RT-PCR analysis. RESULTS: In the results of cDNA microarray we found 117(1.46%) gene differentiations in aged male at least more than 1.0 fold. Among them, the 83 genes were down-regulated and the 34 genes up-regulated. The down expressed genes related to metabolism were 16(19.3%), gene or protein expression 18(21.7%), cell signaling or cell communication 16(19.3%), cell division 19(22.9%), cell structure or motility 6(7.2%) and unknown function 4 genes (4.8%). The up expressed genes related to cell division were 11 (32.4%), gene or protein expression 10(29.4%) and metabolism 3 (8.8%). It is interesting to find that respiratory chain related gene cox7a2 was up-regulated and atp50 down-regulated significantly which as further confirmed by RT-PCR analysis with sequence analysis in the products of the RT-PCR by T-A cloning. CONCLUSION: The gene expression profile in aged male testis was changed significantly as compared with that in normal young controls; testis regression in aging male may relate multi-gene differentiations, especially the differentiations of respiratory chain related gene cox7a2, atp50, which may be an important candidate gene in the study of the mechanism of testis regression in aging male.

Cell Differentiation↗
PubMed2006

Expression profiles of metastatic brain tumor from lung adenocarcinomas on cDNA microarray.

Distant metastasis is one of the crucial parameters determining the type of treatment and prognosis of patients. Previous studies discovered important factors involved in multiple steps of metastasis, the precise mechanisms of metastasis still remain to be clarified. To identify genes associated with this complicated biological feature of cancer, we analyzed expression profiles of 16 metastatic brain tumors derived from primary lung adenocarcinoma (ADC) using cDNA microarray representing 23,040 genes. We applied bioinformatic algorithm to compare the expression data of these 16 brain metastatic loci with those of 37 primary NSCLCs including 22 ADCs, and found that metastatic tumor cells has very different characteristics of gene expression patterns from primary ones. Two hundred and forty-four genes that showed significantly different expression levels between the two groups included plasma membrane bounding proteins, cellular antigens, and cytoskeletal proteins that might play important roles in altering cell-cell communication, attachment, and cell motility, and enhance the metastatic ability of cancer cells. Our results provide valuable information for development of predictive markers as well as novel therapeutic target molecules for metastatic brain tumor of ADC of the lung.

Adenocarcinoma↗
PubMed1995

[Immunology of tuberculosis and cytokines].

One of the unique features characterizing human tuberculosis (TB) is its pathogenesis. The pathogenesis of TB involves cell-mediated immune responses against Mycobacterium tuberculosis. Concisely, macrophages activated by various soluble mediators or cytokines released through the cellular interactions after infection with M. tuberculosis play a pivotal role in the pathogenesis of human TB. In fact, very complex cellular interactions are going on within the host after infection with or endogenous reactivation of M. tuberculosis. Cells communicate by cell-cell contact and by the release of mediators which may originate locally, called cytokines. In TB infection, macrophages can be activated by two ways; directly with mycobacterial organisms or lipid fractions of their cell walls at the earlier phase of infection, and indirectly with cytokines produced by CD4+ T cells specifically activated by mycobacterial peptide antigens at the later phase of infection. The various clinical features of TB are the summarized outcome of cell to cell interactions mediated by diverse cytokines produced by various immune cells which are initially triggered by M. tuberculosis infection. CD4+ T cells can be classified into two subsets according to the patterns of cytokines they produce; Th1 cells give rise to cell-mediated immunity and are characterized by the production of IL-2 and IFN-gamma, whereas Th2 cells are more efficient in mediating antibody production and secrete IL-4, IL-5, IL-6 and IL-10. Th2 cells can control Th1 cells and vice versa. Th2 cells therefore inhibit the production of cytokines by Th1 cells by releasing IL-4 and IL-10. Infection with mycobacteria stimulates macrophage IL-12 production which appears to act directly on naive CD4+ T cells to induce Th1 development and initiation of cell-mediated immunity. IL-12 is a critical component in the development of cell-mediated immunity. In addition, IL-12 also activates NK cells and gamma/delta T cells, both of which secrete various macrophage-activating factors to kill M. tuberculosis. One of the structural characteristics of M. tuberculosis is the cell wall rich in lipid components. Of importance among various biological activities of the cell wall lipids is the stimulation of mononuclear phagocytes to produce a certain number of cytokines or monokines including IL-12 and IL-10, both of which play important roles in regulation of immune responses in mycobacterial infection and in pathogenesis of TB.(ABSTRACT TRUNCATED AT 400 WORDS)

Cytokines↗
PubMed1994

Cellular communications and cell-matrix interactions in the pathogenesis of fibroproliferative diseases: liver fibrosis as a paradigm.

In vitro and in vivo studies suggest a strong cooperation between hepatocytes and mesenchymal cells and between the different non-parenchymal cell types in liver injury and fibrogenesis. The fibrogenic reaction might be described as a dynamic cascade of mechanisms beginning with hepatocyte necrosis and followed by inflammation, activation of macrophages, release of fibrogenic mediators, activation of fat-storing cells, stimulated extracellular matrix synthesis, and diminished matrix degradation resulting in a net matrix accumulation. In detail the initial events of hepatocyte injury and necrosis are followed by local proliferation of Kupffer cells, by influx of blood macrophages and by an aggregation of platelets in necroinflammatory areas. Through phagocytosis and endotoxin challenge, macrophages are activated and convert molecular oxygen into radicals and hydrogen peroxide which might be deleterious to hepatocytes. Furthermore, activated Kupffer cells and degranulating platelets release a number of polypeptide growth regulators stimulating thus fat-storing cell proliferation (transforming growth factor (TGF) alpha/epidermal growth factor, platelet-derived growth factor), transformation into myofibroblasts (transforming growth factor beta, tumor necrosis factor (TNF) alpha) and extracellular matrix synthesis of fat-storing cells and myofibroblasts (TGF-beta, TGF-alpha TNF-alpha). An impressive amount of literature exists demonstrating the central role of fat-storing cells and of its transformed counterpart, ie the highly active and synthetic myofibroblasts in fibrogenesis. These cells produce the majority of the extracellular matrix components, eg collagens, proteoglycans, glycoproteins, and hyaluronan. They have the ability to stimulate themselves via production of growth regulators in an autocrine way. The multiple interactions of the different cells involved in fibrogenesis, the findings that combinations of growth regulators may act additively, synergistically or antagonistically, the fact that certain growth regulators induce the synthesis or receptor expression of others and even of themselves and, findings suggesting an interaction between growth regulators, cell surface receptors, binding proteins (scavengers) and extracellular matrix components indicate a very complex network in fibrogenesis. To get further inside these complicated mechanisms, experimental designs that provide better images of the in vivo situation than conventional techniques used presently are required.

Adipocytes↗
PubMed1999

Cutting edge: protective effects of notch-1 on TCR-induced apoptosis.

The Notch receptor protein was originally identified in Drosophila and is known to mediate cell to cell communication and influence cell fate decisions. Members of this family have been isolated from invertebrates as well as vertebrates. We isolated mouse Notch-1 in a yeast two-hybrid screen with Nur77, which is a protein that has been shown previously to be required for apoptosis in T cell lines. The data presented below indicate that Notch-1 expression provides significant protection to T cell lines from TCR-mediated apoptosis. These data demonstrate a new antiapoptotic role for Notch-1, providing evidence that, in addition to regulating cell fate decisions, Notch-1 can play a critical role in controlling levels of cell death in T cells.

Animals↗
PubMed1985

Functional modulation of cell coupling: evidence for a calmodulin-driven channel gate.

Much of the capacity of tissues to respond to signals as well integrated systems is due to the existence of direct cell-to-cell communication pathways. This type of communication, usually referred to as cell coupling, is based on the presence of cell-to-cell channels permeable to ions, metabolites, and regulatory compounds. The cell-to-cell channels are located at specialized regions of cell contact known as gap junctions or communicating junctions. An important aspect of cell coupling is channel permeability modulation. In recent years this feature of cell coupling has received a great deal of attention, most efforts being aimed at identifying uncoupling treatments and uncoupling agents and at determining the elements of the channel gating mechanism. This review focuses on recent studies suggesting the participation of calmodulin-like proteins in channel gating and on the application of in vitro approaches to cell coupling research-the study of permeability and gating of cell-to-cell channels incorporated into liposomes and the determination of conformational changes in isolated channel protein.

Amino Acid Sequence↗
PubMed1996

Expression pattern of different gap junction connexins is related to embryo implantation.

Successful implantation in mammals requires a close interaction between the embryo and the uterus. Direct cell-cell communication via gap junctions seems to play an important role in the preparation of the uterus for embryo implantation and in the regulation of trophoblast invasion. During preimplantation in the rat the gap junctional proteins connexin (cx) 26 and cx43 are suppressed. This loss of cell-cell communication seems to be important for transformation of the endometrium into the receptive phase. The suppressive effect is mediated by progesterone as demonstrated by the application of antigestagens. At implantation, however, a spatial and temporal pattern of connexin expression is induced in response to embryo recognition. cx26 is locally expressed in the uterine epithelium of the implantation chamber, cx43 in the surrounding decidua prior to invasion. With progressing invasion, the decidual cells surrounding the invading trophoblast in addition to cx43 reveal cx26. In this phase, the invasive partner, the blastocyst, is characterized by coexpression of cx43 and cx31. During trophoblast invasion however, cx31 becomes restricted to the cells of the invasive ectoplacental cone, cx43 to the embryo proper. It seems that compartmentalization of the trophoblast and the inner cell mass is established by two different connexins. During placental differentiation connexin expression switches from cx31 to cx26 and cx43, indicating the end of the invasive phase. The highly regulated pattern of connexin expression in the endometrium as well as in the trophoblast suggests a key role of this different intercellular pathways in regulating the invasion process of the trophoblast into its host tissue, the endometrium.

Animals↗
PubMed1984

Intercellular communication and the control of growth: XI. Alteration of junctional permeability by the src gene in a revertant cell with normal cytoskeleton.

To learn whether the reduction of cell-to-cell communication in transformation is a possible primary effect of pp60src phosphorylation or secondary to a cytoskeletal alteration, we examined the junctional permeability in transformed cells with normal cytoskeleton. The permeability to fluorescent-labelled mono- and diglutamate was compared in clones of Faras' vole cells--clones transformed by Rous sarcoma virus and reverted from that transformation. One revertant clone (partial revertant), had the high level of pp60src kinase activity and tumorigenicity of the fully transformed parent clone, but had lost the cytoskeletal alterations of that clone. Another revertant clone (full revertant) had lost the tumorigenicity and most of the pp60src kinase activity, in addition (J.F. Nawrocki et al., 1984, Mol. Cell Biol. 4:212). The junctional permeability of the partial revertant with normal cytoskeleton was similar to that of the fully transformed parent clone with abnormal cytoskeleton. The permeabilities of both were lower than those of the full revertant and the normal uninfected cell, demonstrating that the junctional change by the src gene is independent of the cytoskeletal one.

Animals↗
PubMed1996

Induction of gap junctional intercellular communication by vitamin D in human skin fibroblasts is dependent on the nuclear Induction of gap junctional intercellular communication by vitamin D in human skin fibroblasts is dependent on the nuclear vitamin D receptor.

The physiologically active metabolite of vitamin D, 1alpha,25-dihydroxyvitamin D3 (calcitriol), induces gap junctional intercellular communication in human skin fibroblasts 161BR at a concentration of 10(-7) M. In human skin fibroblasts, FIB5, devoid of a functional nuclear vitamin D receptor (VDR), there is no effect on gap junctional intercellular communication. Parallel to the increase in cell-cell communication, we observed a VDR-dependent increase in connexin43 protein and connexin43 mRNA levels. These results suggest that 1alpha,25-dihydroxyvitamin D3 affects gap junctional intercellular communication at the level of transcription or of mRNA stability via the nuclear VDR.

Calcitriol↗
PubMed1977

Superiority of adriamycin-14-octanoate over adriamycin in reducing viability of methotrexate-resistant L5178Y cells: brief communication.

Adriamycin-14-octanoate (ADR-OCT) was superior to adriamycin (ADR) in reducing the viability of L5178Y cells resistant to methotrexate (MTX). This effect was seen in logarithmically growing and plateau-phase cultures and increased both with dose and duration of exposure. Both ADR-OCT and ADR were effective inhibitors of the exogenous Escherichia coli DNA-dependent RNA polymerases in vitro and of the endogenous polymerase in mammalian cultured cells. Drug concentrations required for approximately 50% enzyme inhibition in both systems were comparable for both agents, being of the order of 10(-5) M. These experimental studies suggested that ADR-OCT may be a valuable agent for treating neoplasms resistant to MTX.

Animals↗
PubMed1978

Fluorescent probe study of DNA conformation in briefly heated human squamous cells: brief communication.

To determine whether temperature levels commonly encountered in hot beverages denatured the DNA of intact human squamous cells, a fluorescent probe and model system with trypsin-treated desquamated buccal cells were employed. The probe statistically distinguished between single- and double-stranded DNA in a population of suspended cells by the differential bond strengths of DNA-acriflavine complexes over a 4--25 degrees C temperature gradient. The fluorescence of complexed dye was quenched and that of freed dye was restored, which simplified analysis. After cell pellets were admixed with small volumes of suspension medium preheated to 70 or 80 degrees C for 6 seconds, quickly cooled, and stained with acriflavine under conditions favoring the intercalative mode of binding, a temperature-dependent increase occurred in the fraction of complexed dye that was released over the 4--25 degrees C test range. This increase suggested that brief heating partially denatured the DNA of human buccal squamous cells.

Acriflavine↗
PubMed2000

Acyl-homoserine lactone quorum sensing in gram-negative bacteria: a signaling mechanism involved in associations with higher organisms.

Recent advances in studies of bacterial gene expression have brought the realization that cell-to-cell communication and community behavior are critical for successful interactions with higher organisms. Species-specific cell-to-cell communication is involved in successful pathogenic or symbiotic interactions of a variety of bacteria with plant and animal hosts. One type of cell-cell signaling is acyl-homoserine lactone quorum sensing in Gram-negative bacteria. This type of quorum sensing represents a dedicated communication system that enables a given species to sense when it has reached a critical population density in a host, and to respond by activating expression of genes necessary for continued success in the host. Acyl-homoserine lactone signaling in the opportunistic animal and plant pathogen Pseudomonas aeruginosa is a model for the relationships among quorum sensing, pathogenesis, and community behavior. In the P. aeruginosa model, quorum sensing is required for normal biofilm maturation and for virulence. There are multiple quorum-sensing circuits that control the expression of dozens of specific genes that represent potential virulence loci.

4-Butyrolactone↗
PubMed2003

Targeting connexin43 expression accelerates the rate of wound repair.

The repair of tissue damage is a key survival process in all organisms and involves the coordinated activation of several cell types. Cell-cell communication is clearly fundamental to this process, and a great deal is known about extracellular communication within the wound site via cytokines. Here we show that direct cell-cell communication through connexin 43 (Cx43) gap junction channels also plays a major role in the wound healing process. In two different wound healing models, incisional and excisional skin lesions, we show that a single topical application of Cx43 antisense gel brings about a transient downregulation of Cx43 protein levels, and this results in a dramatic increase in the rate of wound closure. Cx43 knockdown reduces inflammation, seen both macroscopically, as a reduction in swelling, redness, and wound gape, and microscopically, as a significant decrease in neutrophil numbers in the tissue around the wound. One long-term consequence of the improved rate of healing is a significant reduction in the extent of granulation tissue deposition and the subsequent formation of a smaller, less distorted, scar. This approach is likely to have widespread therapeutic applications in other injured tissues and opens up new avenues of research into improving the wound healing process.

Animals↗