Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: KEGG:D06522 (Silica)
2,396 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute monocytic leukemia cell line, THP-1, is frequently used as a model to study the mechanism of cell-mediated immune response. The model is justified, in part, because THP-1 cells can be induced to express features of activated peripheral blood monocytes or tissue macrophages. The current investigation, however, demonstrates that THP-1 cells differ from normal monocytes in their secretion of interleukin-1 beta (IL-1 beta) following exposure to reagents that induce synthesis. For example, LPS treatment alone did not result in IL-1 beta secretion and very low concentrations were observed when lipopolysaccharide (LPS)-treated cells were simultaneously incubated with silica or silica in combination with hydroxyurea. Silica-enhanced release of IL-1 was related to changes in cell membrane permeability. Recombinant interferon-gamma (rIFN gamma) alone did not induce IL-1 beta secretion and did not significantly increase secretion by LPS- and silica-stimulated cells. In contrast, mezerein stimulation led to higher extracellular concentrations of IL-1 beta and rIFN gamma augmented secretion by mezerein-treated cells. Isoelectrofocusing of conditioned medium and titration of pooled fractions showed a direct correlation between extracellular levels of biologically active and immunoreactive IL-1. The role of IFN gamma in stimulating IL-1 beta secretion was not related to an enhancement of viability or an increase in the proportion of mezerein-treated cells synthesizing DNA. It was concluded that mezerein's regulation of secretion by THP-1 cells depended on the expression of monocyte features, including cell adherence and responsiveness to IFN gamma.
...
PMID:Secretion of interleukin-1 beta by a leukemia cell line in response to lipopolysaccharide and mezerein. 211 75

The fprA gene is immediately adjacent to the csgA gene (formerly known as spoC) of Myxococcus xanthus. Whereas the csgA gene has an essential role in cell interactions during the developmental cycle, the function of the fprA gene is unknown. Gene disruption was used to determine what affect a null mutation in this gene has on the phenotype of the cell. A csgA-fprA deletion and an fprA frameshift mutation were constructed in vitro in a cloned copy of this locus and then inserted into the M. xanthus chromosome to create a merodiploid with the wild-type and mutant alleles in tandem. The merodiploid was then allowed to segregate one of the two alleles along with the vector sequences in an effort to replace the wild-type allele with the mutant allele. All of the segregants had the wild-type allele, suggesting that a functional fprA gene is essential for vegetative growth. The fprA gene was placed under control of the lacZ transcriptional and translational signals and overexpressed in Escherichia coli, and the new host was examined for any phenotypic changes. A 27-kilodalton protein was observed in sodium dodecyl sulfate-polyacrylamide gels of total-cell protein as predicted from the DNA sequence of this gene. Overexpression of FprA caused the accumulation of a yellow pigment with spectral and redox properties similar to that of the flavins. The pigment cochromatographed with flavin mononucleotide by Silica Gel G thin-layer chromatography. Approximately two-thirds of the total cellular flavin was associated with soluble protein. The major soluble flavin-associated protein was purified on DEAE-Bio-Gel A and Phenyl-Sepharose CL-4B and by polyacrylamide gel electrophoresis. The amino acid composition of the purified protein was similar to that predicted from the DNA sequence of the FprA fusion protein. Apparently, overproduction of FprA (for flavin-associated protein A) in E. coli resulted in a large increase in flavin biosynthesis. Together, these results suggest that the fprA gene encodes a protein that is associated with flavin mononucleotide and has an essential function in M. xanthus.
...
PMID:The Myxococcus xanthus FprA protein causes increased flavin biosynthesis in Escherichia coli. 215 2

Foamy alveolar macrophages (FAM) are observed in lungs injured by Bleomycin (BLM), but their relation to pulmonary fibrosis is not clearly understood. We purified FAM from BLM-instilled rat lungs by density gradient centrifugation on Percoll, and studied the effect of FAM on pulmonary fibrosis. The cells lavaged from the rat lungs 14 days after the administration of BLM (B) or saline (S), were applied on Percoll. After centrifugation, the cells layered on each interface were collected and named as SI, SII, SIII, and BI, BII, BIII in order of gravity. The BI layer included 8.5% of unfractionated cells (U). These BI cells were viable (88%), significantly larger than the others, nonspecific esterase positive cells, and included much ferritin and lysozyme, and were morphologically identified as alveolar macrophages (AM). Therefore, we called the BI cells FAM. We estimated the capacity of FAM (2.5 X 10(5] to synthesize DNA (3H-thymidine uptake) and RNA (3H-uridine uptake), and the activities of silica-stimulated FAM to cause proliferation of mouse thymocytes (IL-1 activity) and rat lung fibroblasts (FP activity), and to produce PGE2. FAM has a lower mitogenic activity but did not have been protein synthetic activity as compared with the others. Silica-stimulated FAM released less IL-1 than BII or BIII, and induced less fibroblast growth than BII, but induced as much as BIII, possibly because of the increased capacity of BIII cells to produce PGE2, which is known to inhibit fibroblast growth. In this way, FAM were considered to be "already activated" rather than "highly activated" cells, but the presence of FAM suggested that smaller or denser AM might receive bleomycin stimulation and release fibrogenic mediators (IL-1 or MDGF) into the alveolar spaces during FAM formation, and that AM might participate in the fibrogenic responses.
...
PMID:[The effect of foamy alveolar macrophages presented in bleomycin-injured rat lungs in pulmonary fibrosis]. 247 35

Male Sprague-Dawley rats were subjected to a single, intratracheal instillation of 30 mg Min-U-Sil silica in sterile saline and were sacrificed 3, 7, or 14 days following instillation. Control animals were instilled with sterile saline only. Silica instillation produced an inflammatory reaction followed by histological changes characteristic of lung fibrosis. Thickened alveolar septa associated with inflammatory cells transforming into large multifocal fibrotic nodules were detected in silica-exposed animals. Increased numbers of bronchoalveolar cells (principally macrophages), elevated levels of protein (principally serum albumin), and lysozyme, proteolytic (trypsin-like), and myeloperoxidase activities were detected in lavage fluids obtained from animals instilled with silica. These factors (except for lysozyme activity) were elevated above control levels from 3 to 7 days postinstillation and declined to near control levels by Day 14. The rate of DNA, collagen, and noncollagen protein synthesis was significantly elevated in lung tissue minces from silica-treated rats 3 and 7 days after instillation. Elevated levels of total protein, and lung collagen in particular, were observed 9 weeks after insult. Lavage fluid from silica-instilled rats stimulates DNA synthesis in cultures of proliferating and quiescent rat lung fibroblasts. Lavage fluid from silica-instilled rats also stimulates lung fibroblasts to increase collagen and noncollagen protein synthesis.
...
PMID:Regulation of lung fibroblast proliferation and protein synthesis by bronchiolar lavage in experimental silicosis. 301 63

Silica or volcanic ash (VA) was administered to rats via intratracheal instillation and the changes in extracellular (i.e., lavage fluid) and tissue phospholipids, as well as various biochemical parameters, were monitored over a 6-month period. VA produced relatively minor (up to 2.8-fold) increases in lung tissue or lavage fluid phospholipids that were maximal at 1 month postinstillation. These increases were quantitatively similar to the increases in protein and DNA content of lung tissue and lavage fluid induced by VA and, thus, may be attributable to hypercellularity and accumulation of cellular breakdown products in the alveolar lumen. Instillation of silica produced a much greater (up to 11-fold) increase than VA in total phospholipid over time, primarily due to a 14-fold increase in phosphatidylcholine (PC). The accumulation of PC was more pronounced in the lavage fluid during the first month following silica instillation, but thereafter progressed more rapidly in the lung tissue. The relatively small increases (1.3- to 3.5-fold) in other phospholipids induced by silica appeared to be nonspecific, since they did not differ greatly from the increases in lung weight, DNA, and protein. Collectively, these results indicate that intratracheal instillation of silica induces selective accumulation of lung PC, implying enhanced synthesis and secretion of pulmonary surfactant from alveolar epithelial Type II cells into the lumen.
...
PMID:Effect of silica and volcanic ash on the content of lung alveolar and tissue phospholipids. 609 47

Some unique events have occurred in the last few years which might revolutionize the field of polyacrylamide gel electrophoresis. While it was widely recognized that such matrices could normally be cast with a small pore size distribution, typically of the order of a few nanometers diameter (for protein sieving), recent developments suggest that "macroporous" gels could also be produced in the domain of polyacrylamides. If constraints to chain motion are imposed during gel polymerization, large-pore structures can be grown. Such constraints can originate either from low temperatures or from the presence of preformed polymers in the gelling solution; in both cases, the growing chains are forced to "laterally aggregate" via inter-chain hydrogen bond formation. Upon consumption of pendant double bonds, such bundles are frozen in the three-dimensional space by permanent cross-links. As an additional development, a novel photopolymerization system is described, comprising a cationic dye (methylene blue) and a redox couple (sodium toluene sulfinate, a reducer, and diphenyliodonium chloride, a mild oxidizer). Methylene blue catalysis is characterized by a unique efficiency, ensuring >96% conversion of monomers, even in hydro-organic solvents and in the presence of surfactants, which normally quench or completely inhibit the persulphate-driven reaction. In addition, methylene blue-sustained photopolymerization can be operated in the entire pH 3-10 interval, where most other systems fail. Perhaps the most striking novelty in the field is the appearance of a novel monomer (N-acryloylaminopropanol, AAP) coupling a high hydrophilicity with a unique resistance to alkaline hydrolysis. Given the fact that a poly(AAP) matrix is 500 times more stable than a poly(acrylamide) gel, while being twice as hydrophilic, it is anticipated that this novel chemistry will have no difficulties in replacing the old electrophoretic anticonvective media. The review ends with a glimpse at novel sieving media in capillary zone electrophoresis: polymer networks. Such media, by providing an almost infinite range of pore sizes, due to the absence of a rigid support, allow sieving mechanisms to be operative over a wide interval of particle sizes, even up to genomic DNA. Viscous solutions of polymer networks, made with the novel poly(AAP) chemistry, allow repeated use of the same separation column, well above 50 injections. Silica-bound poly(AAP) chains provide effective quenching of electroosmosis and >200 analyses by isoelectric focusing.
...
PMID:Electrophoresis gel media: the state of the art. 939 68

Silica exposure results in an initially acute inflammatory response followed by chronic fibrotic change. The mechanism for the maintenance of silica-induced inflammation has not been understood yet. In silica-induced acute inflammation and chronic fibrosis, various mediators such as reactive oxygen species, cytokines and growth factors are released. And these substances are suggested to have the regulatory role for the inflammation and fibrosis by possessing the potential to influence apoptosis. To demonstrate the apoptosis as an underlying mechanism for the development of silicosis, in vitro and in vivo models were designed. In in vitro study, we evaluated that apoptotic cell fraction in silica (10, 50 microg/cm2)-treated A549 cells was significantly increased in comparison with control by FACS (fluorescein activated cell sorter). Also genomic DNA from silica (10, 50 microg/cm2)-treated A549 showed DNA ladder formation while control and 1 microg/cm2 groups didn't. In in vivo study, total cell numbers and apoptotic cell numbers of BAL (bronchoalveolar lavage) fluid from silica (10, 20, 40 mg/kg)-instilled rats were significantly higher than control group from 1 week. From these results, we concluded acute and chronic presence of apoptosis may contributes to silica-induced acute inflammation and chronic fibrosis.
...
PMID:Silica-induced apoptosis in vitro and in vivo. 1051 Dec 80

The main objective of this study was to evaluate the critical role of glutathione (GSH) in silica-induced oxidative stress, cytotoxicity, and genotoxicity in rat alveolar macrophages (AMs). Silica-induced superoxide radical and hydrogen peroxide formation were determined with lucigenin-dependent chemiluminescence and 2', 7'-dichlorofluorescin diacetate fluorescence test, respectively. The cytotoxicity of silica was estimated by lactate dehydrogenase leakage, and a comet assay was used for examining silica-induced DNA damage in AMs. The intracellular GSH content was modulated by N-acetylcysteine, a GSH precursor, and buthionine sulfoximine, a specific GSH synthesis inhibitor. It was found that silica led to a dose- and time-dependent decrease in GSH content in AMs. N-acetylcysteine increased intracellular GSH level and protected against silica-induced reactive oxygen species formation, lactate dehydrogenase leakage, and DNA strand breaks in AMs. In contrast, buthionine sulfoximine pretreatment depleted cellular GSH and enhanced the susceptibility of AMs to the cytotoxic and genotoxic effects of silica. It thus appears that GSH plays a critical role in protecting against silica-induced cell injury, most probably through its antioxidant activity.
...
PMID:Critical role of GSH in silica-induced oxidative stress, cytotoxicity, and genotoxicity in alveolar macrophages. 1051 15

Nuclear factor-kappaB (NF-kappaB) is a multiprotein complex that may regulate a variety of inflammatory cytokines involved in the initiation and progression of silicosis. The present study documents the ability of in vitro silica exposure to induce DNA-binding activity of NF-kappaB in a mouse peritoneal macrophage cell line (RAW264.7 cells) and investigates the role of reactive oxygen species (ROS) and/or protein tyrosine kinase in this activation. In vitro exposure of mouse macrophages to silica (100 microg/ml) resulted in a twofold increase in ROS production, measured as the generation of chemiluminescence (CL), and caused activation of NF-kappaB. Silica-induced CL was inhibited 100% by superoxide dismutase (SOD) and 75% by catalase, while NF-kappaB activation was inhibited by a variety of antioxidants (catalase, superoxide dismutase, alpha-tocopherol, pyrrolidine dithiocarbamate, or N-acetylcysteine). Further evidence for the involvement of ROS in NF-kappaB activation is that 1 mM H2O2 enhanced NF-kappaB/DNA binding and that this activation was inhibited by catalase. Specific inhibitors of protein tyrosine kinase, such as herbimycin A, genistein, and AG-494, prevented NF-kappaB activation in silica-treated cells. Genistein and AG-494 also reduced NF-kappaB activation in H2O2-treated cells. Results confirm that tyrosine phosphorylation of several cellular proteins (approximate molecular mass of 39, 58-70, and 103 kD) was increased in silica-exposed macrophages and that genistein inhibited this silica-induced phosphorylation. In contrast, inhibitors of protein kinase A or C, such as H89, staurosporin, calphostin C, and H7, had no marked inhibitory effect on silica-induced NF-kappaB activation. The results suggest that ROS may play a role in silica-induced NF-kappaB activation in macrophages and that phosphorylation events mediated by tyrosine kinase may be involved in this activation.
...
PMID:Silica-induced nuclear factor-kappaB activation: involvement of reactive oxygen species and protein tyrosine kinase activation. 1083 16

Multiple uses for synthetic cationic liposomes composed of dioctadecyldimethylammonium bromide (DODAB) bilayer vesicles are presented. Drugs or biomolecules can be solubilized or incorporated in the cationic bilayers. The cationic liposomes themselves can act as antimicrobial agents causing death of bacteria and fungi at concentrations that barely affect mammalian cells in culture. Silica particles or polystyrene microspheres can be functionalized by coverage with DODAB bilayers or phospholipid monolayers. Negatively charged antigenic proteins can be carried by the cationic liposomes which generate a remarkable immunoadjuvant action. Nucleotides or DNA can be physically adsorbed to the cationic liposomes to be transferred to mammalian cells for gene therapy. An overview of the interactions between DODAB vesicles and some biomolecules or drugs clearly points out their versatility for useful applications in a near future.
...
PMID:Interactions between cationic liposomes and drugs or biomolecules. 1093 2


1 2 3 4 5 6 7 Next >>

---