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At least 1,801 records · Page 100Linked to original sources
PubMed1999

Telomere shortening triggers a p53-dependent cell cycle arrest via accumulation of G-rich single stranded DNA fragments.

It has been repeatedly suspected that telomere shortening might be one possible trigger of the p53-dependent cell cycle arrest, although the mechanism of this arrest remained unclear. Telomeres in human cells under mild oxidative stress accumulate single-strand damage faster than interstitial repetitive sequences. In MRC-5 fibroblasts and U87 glioblastoma cells, which both express wild-type p53, oxidative stress-mediated production of single-strand damage in telomeres is concomitant to the accumulation of p53 and p21 and to cell cycle arrest. This response can be modeled by treatment of cells with short single stranded telomeric G-rich DNA fragments. The arrest is transient in U87 cells. Recovery from it is accompanied by up-regulation of telomerase activity and elongation of telomeres. Overexpression of mutated p53 is sufficient to reverse the phenotype of inhibition as well as the delayed activation of telomerase. These data suggest that the production of G-rich single stranded fragments during the course of telomere shortening is sufficient to trigger a p53 dependent cell cycle arrest.

Adenocarcinoma↗
PubMed1986

Modulation of glycogen metabolism in cerebromicrovascular smooth muscle and endothelial cultures.

The separately cultured smooth muscle and endothelial cells derived from dissociated cerebral microvessels are characterized by high content of glycogen. Norepinephrine induces glycogenolysis while 5-hydroxytryptamine stimulates glycogenesis in both cell types. The endogenous glucose of the endothelium but not that of the smooth muscle serves as a direct source for the 5-HT enhancement of glycogen formation. Indomethacin, the known inhibitor of cyclooxygenase modulates the glycogen content in the smooth muscle only. These findings strongly suggest that the carbohydrate metabolism of each cell has a distinct control mechanism compatible with the underlying integral microvascular function.

Adenosine Triphosphate↗
PubMed1980

Phospholipid composition and heat sensitivity in a thermophilic bacterium.

A Gram-negative thermophilic bacterium designated strain LEH-1, survived under non-growth conditions, temperatures 5 degrees C above its maximum for growth when acetate or n-heptadecane served as carbon source, whereas cells grown with glucose or glycerol were markedly more sensitive to elevated temperatures. The total extractable lipids from strain LEH-1 and the concentrations of phosphatidylethanolamine and phosphatidic acid in the cytoplasmic membranes was altered by the growth substrate. Growth with acetate of n-heptadecane as carbon source yielded cells containing more phosphatidic acid than phosphatidylethanolamine. Conversely, more phosphatidylethanolamine was present in cells following growth with glucose or glycerol as carbon source. The relative amount of specific fatty acids and distribution in major phospholipid moieties was also affected by the growth substrate. These differences in composition may reflect an alteration in the physical properties of the cellular membrane and account for the divergence in heat sensitivity.

Acetates↗
PubMed2004

Macrophages release tumor necrosis factor alpha and interleukin-12 in response to intracellular Bacillus anthracis spores.

Herein we report that infection of a murine macrophage cell line with Bacillus anthracis results in the production of tumor necrosis factor alpha and interleukin-12 (IL-12). When infected with B. anthracis spores in combination with lipopolysaccharide, macrophages release increased amounts of IL-12. We found no evidence of inhibition of cytokine responses in macrophages infected with B. anthracis spores.

Animals↗
PubMed1982

Insertion tendopathy in athletes. A light microscopic, histochemical and electron microscopic examination.

Tendon tissue of eleven athletes suffering from insertion tendopathy and of two controls was examined. Part of the tissue was prepared for routine light microscopy, a part for enzyme histochemical staining of Nicotinamide-adenine-dinudeotide-diaphorase (NADP-diaphorase), lactate dehydrogenase (LDH), beta-glucuronidase and alkaline phosphatase. Small pieces of tissue were also prepared for electron microscopic examination. The removed tissue was edematous and mushy. The normally densely packed parallel or interwoven collagen bundles were loosened by edema, focal necrosis or hemorrhage. Infiltration of fatty tissue and granulation tissue was also present. The amount of acid mucopolysaccharides was markedly increased. The histochemical studies showed strong enzyme activity of NADP-diaphorase and LDH in normal tendon tissue as well as around areas of degeneration and in granulation tissue. beta-Glucuronidase and alkaline phosphatase was present, but in general with lesser activity than the above enzymes. The electron microscopic examination revealed marked degeneration of the fiber systems, focal necrosis, deposit of amorphous masses and mucopolysaccharides and focal mineralisation. The reparative zones showed proliferating capillaries, often with a collapsed lumen and prominent endothelial cells and basement membranes.

Adult↗
PubMed2000

The effects of Cryptococcus neoformans-secreted antigens on tumor necrosis factor-alpha-induced intercellular adhesion molecule-1 expression on human lung epithelial cells.

Since primary infection with Cryptococcus neoformans usually occurs in the lungs, and since pulmonary cryptococcosis involves interactions between yeasts and alveolar epithelial cells, we have begun to study the effects of C. neoformans and its secreted antigens (SA) on epithelial reactions potentially associated with localized inflammation. We report here that SAs from encapsulated and acapsular strains of C. neoformans caused significant reductions in tumor necrosis factor-alpha (TNF-alpha)-induced intercellular adhesion molecule-1 (ICAM-1) expression on A549 lung epithelial cells in culture. We also present evidence that the reduction in ICAM-1 expression was not associated with SA-induced shedding of this adhesion molecule.

Antigens, Fungal↗
PubMed2006

Lipoprotein lipase-facilitated uptake of LDL is mediated by the LDL receptor.

LPL mediates the uptake of lipoproteins into different cell types independent of its catalytic activity. The mechanism of this process and its physiological relevance are not clear. Taking into account the importance of the endothelial barrier for lipoprotein uptake, in vitro studies with primary aortic endothelial cells from wild-type and low density lipoprotein receptor (LDLR)-deficient (LDLR(-/-)) mice were performed. Addition of LPL almost doubled the uptake of LDL into wild-type cells. However, there was virtually no LPL-mediated change of LDL uptake into LDLR(-/-) cells. Upregulation of LDLR by lipoprotein-deficient serum/lovastatin in wild-type cells resulted in a 7-fold increase of LPL-mediated LDL uptake. Uptake of chylomicron remnants was not affected by LDLR expression. In proteoglycan-deficient cells, LPL did not increase the uptake of lipoproteins. The physiological relevance of this pathway was studied in mice that were both LDLR(-/-) and transgenic for catalytically inactive LPL in muscle. In the presence of LDLR, inactive LPL reduced LDL cholesterol significantly (13-24%). In the absence of LDLR, LDL cholesterol was not affected by transgenic LPL. Metabolic studies showed that in the presence of LDLR, LPL increased the muscular uptake of LDL by 77%. In the absence of LDLR, transgenic LPL did not augment LDL uptake. Chylomicron uptake was not affected by the LDLR genotype. We conclude that LPL-mediated cellular uptake of LDL, but not of chylomicrons, is dependent on the presence of both LDLR and proteoglycans.

Animals↗
PubMed1997

The in vitro interaction of Cryptococcus neoformans with human lung epithelial cells.

The interaction of Cryptococcus neoformans with a human lung epithelial cell line (A549) is described. Encapsulated and acapsular strains adhered to epithelial cells in a time-dependent manner, with the acapsular strain being the most adherent under all conditions tested. Internalized cryptococci were additionally observed. The expression of the adhesins responsible for adherence to the epithelial cells was induced by growth at 37 degrees C. Adhesin expression was repressed in all strains by growth with sucrose as the sole carbon source. A strain-specific repression of adhesin expression was observed after growth with galactose and xylose. A variety of carbohydrates included in the assay suspensions blocked adherence, implicating certain carbohydrate moieties that might serve as ligands for the yeast adhesin. Finally, a monoclonal antibody is described that inhibited cryptococcal adherence to the epithelial cells. Collectively, the results demonstrate a specific interaction between C. neoformans and lung epithelial cells mediated by yeast adhesins whose expression is regulated by environmental factors.

Adhesiveness↗
PubMed1989

Conditions affecting the amphotericin B mediated inhibition of Candida albicans attachment to cell cultures.

Sublethal amounts of amphotericin B inhibited the attachment of Candida albicans to cultured mammalian cells. The extent of inhibition was influenced by the concentration of serum and the growth phase of the yeasts used to inoculate the cell cultures. Yeasts which were in their exponential phase of growth or had formed germ tubes were the most sensitive to amphotericin B. Equivalent amounts of amphotericin B inhibited yeast-mammalian cell interactions to different degrees depending upon the culture's tissue origin.

Amphotericin B↗
PubMed1993

Conditions affecting the adherence of Cryptococcus neoformans to rat glial and lung cells in vitro.

Conditions affecting the adherence of clinical isolates of Cryptococcus neoformans to rat glial and lung cell cultures were studied. Adherence to glial cells was a time-dependent process that was affected by the yeast culture age and growth temperature. The most adherent yeasts were those from 48 h cultures grown at 37 degrees C. Formalin-treating the yeasts did not affect adherence but formalin-treating the glial monolayers prevented yeast binding. Treating the yeasts with trypsin reduced adherence to glial monolayers, indicating that the yeast adhesin had a trypsin-labile protein component. Certain carbohydrates inhibited cryptococcal adherence to glial and lung cells in a time and concentration-dependent manner. Of the carbohydrates tested, N-acetyl-D-glucosamine, sucrose, lactose, sorbitol and myo-inositol were the most inhibitory, while mannose, galactose and xylose were the least inhibitory. The results collectively indicated that the mechanisms of adherence of C. neoformans to lung cells were similar to those of glial cells and that both involved a protein-containing adhesin on the cryptococcal surface that was expressed only after growth at 37 degrees C. Carbohydrate receptors also appeared to be involved with these interactions.

Animals↗
PubMed1988

Factors influencing the interaction of Candida albicans with fibroblast cell cultures.

The interaction of Candida albicans clinical isolates with primary and established fibroblast cultures was studied. The intent was to determine whether yeast adherence and invasion of nonendothelial cell monolayer cultures could be quantitated reproducibly and whether this system could be used for future studies on yeast pathogenesis. Our results demonstrated that specific interactions between the yeast cells and fibroblasts only occurred at 37 degrees C and correlated with the germination process. Fluorescent-antibody staining indicated that invasion or tight associations between the germinating yeast cells and mammalian cells occurred after less than 3 h of incubation. Yeast adherence was estimated radiometrically and trypsin-resistant interaction with individual mammalian cells (infection) was measured microscopically after inoculated monolayer cells were detached with trypsin. We demonstrated that both types of association were time dependent at 37 degrees C; neither was affected by the concentration of glucose used to grow the yeast cells. Primary and established fibroblast cell lines were equally susceptible to infection, but primary cells appeared to have more yeast-binding sites. Fibroblasts maintained in confluent culture for an extended period of time also appeared to have more binding sites, and while not quantitatively more susceptible to infection, the older cells were more susceptible to infection-related cell death. An established kidney epithelial cell line (MDCK) was not susceptible to either type of yeast interaction, indicating that the yeast-fibroblast associations were specific.

Animals↗
PubMed1981

Adipocyte size and number in dietary obesity resistant and susceptible rats.

Fat depot cellularity was assessed in overfed dietary obesity resistant S 5B/Pl (S) and susceptible Osborne-Mendel (OM) rats. Cell number and lipid per cell were determined for three fat depots in both 24- and 105-day-old rats. Between these two ages, fat cell number doubled in inguinal fat depots of S rats fed high- or low-fat diets and OM rats fed a low-fat diet, but quadrupled in OM rats fed a high-fat diet. The size of adipocytes in this depot was influenced by strain but not by diet. Compared to normal weight S rats, 24-day-old overfed S rats had twice as many adipocytes in the perirenal-retroperitoneal fat depot. Overfed OM rats had 3 times perirenal-retroperitoneal fat depot. Overfed OM rats had 3 times as many. In OM rats fed the high-fat diet, there was a 16-fold increase in adipocyte number between 24 and 105 days of age. Overfeeding caused a slight increase in perirenal-retroperitoneal adipocyte size in 24-day-old rats but had little influence on cell size in 105-day-old rats.

Adipose Tissue↗
PubMed1998

Purification of untagged retroviral integrases by immobilized metal ion affinity chromatography.

We have developed a simple protocol for the purification of untagged retroviral integrases expressed in bacterial cells. The method takes advantage of the inherent ability of the proteins to bind metal ions. The protocol involves an initial enrichment of the protein in the pellet fraction following centrifugation of the lysate after cell lysis. Integrase is then solubilized from the pellet at high salt conditions (1 M) with detergent and applied to a nickel-charged iminodiacetic acid-Sepharose column. The enzyme is eluted from the column with imidazole. The resulting protein, which is 70-80% homogeneous, is subsequently purified to homogeneity on a heparin-Sepharose column. The two-column protocol is easily completed in a day and yields approximately 2 mg of enzymatically active protein per gram of wet cell paste.

Avian Sarcoma Viruses↗
PubMed1977

Effect of growth substrate on thermal death of thermophilic bacteria.

The heat sensitivity of gram-negative, hydrocarbon-utilizing thermophilic bacteria was altered by a change in growth substrate. Thermophilic strains CC-6, BI-1, and LEH-1, grown with acetate or n-heptadecane as the carbon source, had a higher survival rate when incubated 5 degrees C above their maximum growth temperature than cells of the same organism after growth on glucose or glycerol. There was a correlation between the growth substrated, heat resistance, and the ratios of cellular n-hexadecanoic acid/branched hexadecanoic acid and n-heptadecanoic acid/branched heptadecanoic acid. The bacterial cells that were more heat resistant had ratios of straight-chain/branched-chain fatty acids above 1.0, whereas the heat-sensitive cells had ratios below 0.6.

Acetates↗

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