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At least 19 recordsLinked to original sources
PubMed2003

Mast cell-IgE-and mast cell-structural cell interactions in allergic airway disease.

Allergic diseases like atopic rhinitis, bronchial asthma, and urticaria are prevalent and on the rise. Mast cells are known to play a central role in the immediate phase reaction of allergic diseases through the IgE-mediated release of a variety of chemical mediators like histamine, leukotrienes, and prostaglandins. On the other hand, T lymphocytes, basophils and eosinophils are thought to be responsible in inducing the late phase response. Yet, recent studies show that the mast cell cannot be simplistically assigned a role in the immediate phase allergic response, and that this cell plays a crucial role in ongoing allergic inflammation, including the development of hyper-responsiveness. In the present article, the author will try to discuss the integrated roles of mast cells in IgE-mediated allergic inflammation with specific emphasis on the roles of mast cell-IgE networking and mast cell-structural cell interactions in the late phase allergic response and chronic allergic inflammation.

Asthma↗
PubMed1995

Rethinking cell structure.

Cell structure, emerging from behind the veil of conventional electron microscopy, appears far more complex than formerly realized. The standard plastic-embedded, ultrathin section can image only what is on the section surface and masks the elaborate networks of the cytoplasm and nucleus. Embedment-free electron microscopy gives clear, high-contrast micrographs of cell structure when combined with removal of obscuring material such as soluble proteins. The resinless ultrathin section is the technique of choice; it is simple and inexpensive, and it uses ordinary electron microscopes. The resulting pictures reveal a world of complex cell structure and function. These images necessarily change our conception of the cytoskeleton, nuclear matrix, mitosis, and the relation of membranes to cytostructure.

Animals↗
PubMed1994

Coupling of cell structure to cell metabolism and function.

The fact that cells make directed decisions regarding how to use energy, i.e., where to direct intracellular particles or where to move, suggests that energy can be, and is, harnessed in specific ways. It is now well established that the chemical reactions of the cell do not occur in nonorganized soup, but rather in the context of ordered structure. The physical components that make up this ordered structure of the cell are part of the tissue matrix, which consists of the dynamic linkages between the skeletal networks of the nucleus (the nuclear matrix), the cytoplasm (the cytoskeleton), and the extracellular environment (the extracellular matrix). To understand gene function and how the energy of the cell is directed towards accomplishing the tasks directed by DNA (gene expression), a further understanding of how cell structure is tied to cellular energy and function is required. We propose that the structural components of the cell harness cellular energy to direct cell functions by providing a dynamic bridge between thermodynamics and gene expression.

Animals↗
PubMed1997

High D-glucose induces alterations of endothelial cell structure in a cell-culture model.

Diabetes mellitus leads to micro- and macroangiopathy with endothelial dysfunction. To investigate the direct influence of high glucose on endothelial cell structure and possible pharmacologic effects, seven different experimental protocols were carried out on endothelial cells in culture. There were four control groups with either 5 mM D-glucose alone, 5 mM D-glucose plus 15 mM L-glucose (for osmotic control), 5 mM D-glucose plus 500 nM celiprolol, or 5 mM D-glucose plus 57 nM nitrendipine. Three experimental groups had either 20 mM D-glucose alone, 20 mM D-glucose plus 500 nM celiprolol or 20 mM D-glucose plus 57 nM nitrendipine. Treatment of all groups started at the third passage of the cells and lasted until confluence was reached (5-8 days). The endothelial cells were fixed in paraformaldehyde and stained either with hematoxylin-eosin solution, with nitro blue tetrazolium for nicotinamide adenine dinucleotide phosphate (NADPH)- diaphorase staining, or actin staining with phalloidin was carried out. For quantitative analysis of the histologic specimens, the slides were viewed via a microscope and a videocamera. The pictures were converted digitally and could be analyzed with the videopicture-analyzing system, JAVA. In the four control groups, neither treatment with 15 mM L-glucose nor administration of celiprolol or nitrendipine had an effect on cell, cytoplasm, and nuclear area. The number of giant or polynuclear cells and the histochemical NADPH-diaphorase activity were not altered. Incubation of endothelial cells with 20 mM D-glucose for 5-8 days resulted in a significant increase in total and cytoplasmic area, as well as in the number of giant and polynuclear cells, whereas the nuclear area and the NADPH-diaphorase activity were significantly reduced. Concomitant treatment with celiprolol was able to reverse these alterations in endothelial structure significantly but had only a weak effect on the NADPH-diaphorase. Nitrendipine had no beneficial effect on the high D-glucose-induced cell alterations. The actin staining of the control cells showed the typical actin pattern with most of the actin filaments arranged at the periphery of the cells. Administration of 20 mM D-glucose resulted in a disturbance of the actin pattern, with most of the actin filaments now arranged in the middle of the cells. However, neither celiprolol nor nitrendipine exhibited a significant influence on this altered actin structure. High D-glucose treatment over several days thus leads to severe changes in endothelial cell structure, and celiprolol may have a beneficial effect on these hyperglycemia-induced cell alterations.

Actins↗
PubMed1990

Cancer cell structure: actin changes in tumour cells--possible mechanisms for malignant tumour formation.

Improvement in treatment of solid tumours is likely to depend on a better knowledge of the biological mechanisms of malignant tumour formation. Over the past few years a great deal of progress has occurred in our understanding of cell biology, and one of the main areas of development has been the cell cytoskeleton. The cytoskeleton contributes to maintenance of cell structure and to a variety of other cell functions. Several studies have implicated one of the elements of the cytoskeleton, the microfilaments, in malignant change, and these microfilaments are directly affected by the activity of some 'oncogenes'. Changes in the control of filament polymerization and organization have been demonstrated in response to the activity of the src oncogene. The protease trypsin has been shown to affect the actin cytoskeleton grossly and illustrates that proteases released in the vicinity of tumours may have a biologically significant effect on the internal structure and stability of the cell. Further investigation of the microfilament system may reveal important clues for future manipulation of the cancer cell and the treatment of the patient with advanced cancer.

Actins↗
PubMed1997

Stem cell factor in nasal polyposis and allergic rhinitis: increased expression by structural cells is suppressed by in vivo topical corticosteroids.

BACKGROUND: Mast cells are increased in nasal polyp (Np) and allergic rhinitis (AR) tissue and are suppressed by topical corticosteroid treatment. Stem cell factor (SCF), a mast cell growth and survival factor, may explain these phenomena. OBJECTIVE: We investigated structural cell gene expression and production of SCF in nasal tissues in patients who had received and who had not received in vivo intranasal corticosteroid therapy. METHODS: Northern blot analyses for messenger RNA and ELISA for biologically active SCF protein from cultured Np epithelial cells and fibroblasts were performed. Immunostaining for SCF in cultured and tissue nasal structural cells in the presence or absence of steroid treatment was also performed. RESULTS: We detected significant expression of SCF mRNA and protein by cultured Np epithelial cells and Np fibroblasts; Np fibroblast SCF supported the differentiation of mast cells in vitro. There were more immunoreactive SCF-positive Np epithelial cells in patients with AR than in control subjects (97.2 +/- 2.8 vs 45.6 +/- 22.0%; p < 0.0001). SCF that could be immunostained was significantly diminished overall in Np structural cells in the group given in vivo steroid treatment, with a modest (trend to significant) effect on any given cell type analyzed. In vitro treatment with budesonide of SCF-producing fibroblasts demonstrated inhibition of unstimulated, primary Np fibroblasts but not of IL-1-stimulated fibroblasts or transformed cell lines. CONCLUSIONS: Human Np and AR tissue structural cells express and produce increased SCF. Our in vitro studies suggest that intranasal steroids blunt SCF expression in Nps, an effect that may be responsible for a decrease in mast cells and symptoms.

Administration, Topical↗
PubMed1993

Characteristic and differential calcium signals from cell structures of the root cap detected by energy-filtering electron microscopy (EELS/ESI).

Characteristic calcium signals were analyzed in structures of three cell types of the root cap of cress: statocytes, meristematic cells and secretion cells. Twenty-four hour-old roots were fixed with glutaraldehyde (postfixed with osmiate/potassium bichromate) or with potassium permanganate. No visible precipitates were formed, but calcium signals typical for different cell structures could be detected by means of energy-filtering transmission electron microscopy (EELS/ESI). In statocytes, calcium signals were recorded from the plasma membrane, the membranes of the endoplasmic reticulum, the amyloplast envelope and the mitochondrial membranes. In contrast to the excitable statocytes, the two other, non-excitable cell types, meristematic and secretion cells, exhibited much lower intensities of the calcium signals recorded from the same membrane systems. The revealed characteristic calcium-related properties of the different membrane systems may be related to the special function of statocytes, namely transduction of the gravity stimulus. In all three cell types, additional calcium signals were recorded from cell structures with well known calcium contents, i.e., mitochondrial granules, starch grains and cell walls. For the first time, clear calcium signals were detected from the lipid bodies which are mobilized during the developmental stage of the examined roots. It is supposed that free fatty acids and lipases are the binding sites for calcium. The reliability of the applied method is especially proven by comparison of the electron microscopic images from lipid bodies according to the two different fixation methods. After glutaraldehyde fixation followed by osmiate/potassium bichromate postfixation, the lipid bodies were well fixed and appeared homogeneously grey with homogeneous calcium signals. However, due to potassium permanganate fixation the lipid bodies were only partly fixed; they had an electron-lucid core, from which the lipids are lost during the dehydration procedure, without calcium signals and an electron-dense border zone, which is a reaction product of potassium permanganate with triacylglycerols, with calcium signals.

Calcium↗
PubMed1989

The role of calmodulin in rat parotid amylase secretion: effects of calmodulin antagonists on secretion and acinar cell structure.

Using dispersed rat parotid cells, the effects of three calmodulin antagonists, trifluoperazine (TFP), N-(6-aminohexyl)-5-chloro-1-naphthalensulfonamide (W-7), and N-(6-aminohexyl)-1-naphthalenesulfonamide (W-5), on amylase release and acinar cell structure were examined. TFP and W-7 strongly inhibited both isoproterenol (ISO)- and dibutyryl cyclic AMP-stimulated amylase release at a concentration of 50 or 100 microM, while W-5, a weak calmodulin antagonist, had only little effect. Cyclic AMP level was markedly elevated by ISO even in the presence of TFP or W-7. These results indicate that the calmodulin antagonists affect amylase release at steps distal to cyclic AMP metabolism. Electron micrographs demonstrated that treatment of parotid cells with either TFP or W-7 caused a loss of luminal microvilli and surface folds. When cells were stimulated by ISO in the presence of TFP or W-7, the enlarged lumina did not recover to their original size and the discharged secretory material was retained in the lumina. Numerous secretory granules remained in the acinar cytoplasm. W-5 affected the acinar cell structure only a little. These observations lead to the assumption that TFP and W-7 interfered with the normal functions of the cytoskeletal system. It is proposed that calmodulin may be involved in the exocytosis of parotid amylase through the regulation of the cytoskeletal system.

Amylases↗
PubMed1975

The fine structure of proliferating cartilage cells: structural changes in an experimental model.

Extensive development of the rough endoplasmic reticulum and comparatively less developed Golgi membranes were seen in the cells of chondrocyte clusters which had formed in the vicinity of cartilage defects produced by intra-articular papain and cortisone injections. These cells frequently showed myelin-like membranous figures. These figures were seen either close to the cell membrane, or between cells, or connected to the nuclear envelope or the endoplasmic reticulum. The hypothesis is advanced that the myelin figures are made from redundant material which was not used for membrane formation. Cortisone, which is known to interfere with mitochondrial function and general metabolic processes, could have been responsible for the deficiency in membrane differentiation and transfer. This investigation was supported by grants from the Orthopaedic Research and Education Foundation and from the Research Evaluation and Allocation Committee of the School of Medicine, Univeristy of California, San Francisco.

Animals↗
PubMed2003

The three-dimensional architecture of the notochordal nucleus pulposus: novel observations on cell structures in the canine intervertebral disc.

Cells from the nucleus pulposus of young (< 2 years) and old (> 5 years) non-chondrodystrophoid dogs were studied using routine histology, confocal laser scanning microscopy and transmission electron microscopy. The architecture of cell structures--from the tissue scale down to subcellular scale--was reported. Clusters of notochordal cells were observed in young nuclei pulposi, ranging from 10 to 426 cells each. These clusters resisted mechanical disruption and showed evidence of cell-cell signalling via gap junctions. Cells (30-40 microm in diameter) within the clusters had a physaliferous appearance, containing numerous large inclusions which ranged from 1 to 20 microm in diameter. The inclusions were surrounded by a dense actin cortex but were not contained by a lipid bilayer. The contents of the inclusions were determined not to be predominantly carbohydrate or neutral lipid as assessed by histochemical staining, but the exact composition of the contents remained uncertain. There were striking differences in the cell architecture of young vs. old nuclei pulposi, with a loss of both cell clusters and physaliferous cells during ageing. These observations demonstrate unique cell structures, which may influence our understanding of the differences between notochordal and chondrocytic cells in the nucleus pulposus. Such differences could have substantial impact upon how we think about development, degeneration and repair of the intervertebral disc.

Aging↗