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At least 19 recordsLinked to original sources
PubMed1989

Characterization of cytosolic forms of CTP: choline-phosphate cytidylyltransferase in lung, isolated alveolar type II cells, A549 cell and Hep G2 cells.

The subcellular forms of cytidylyltransferase (EC 2.7.7.15) in rat lung, rat liver, Hep G2 cells, A549 cells and alveolar Type II cells from adult rats were separated by glycerol density centrifugation. Cytosol prepared from lung, Hep G2 cells, A549 cells and alveolar Type II cells contained two forms of the enzyme. These species were identical to the L-Form and H-Form isolated previously from lung cytosol by gel filtration. Liver cytosol contained only the L-Form. Rapid treatment of Hep G2 cells with digitonin released all of the cytoplasmic cytidylyltransferase activity. The released activity was present in both H-Form and L-Form. The molecular weight of L-Form was determined from sedimentation coefficients and Stokes radius values to be 97,690 +/- 10,175. Thus, the L-Form appears to be a dimer of the Mr 45,000 catalytic subunit. The f/f degrees value of 1.5 indicated that the protein molecule has an axial ratio of 10, assuming a prolate ellipsoid shape. The estimated molecular weight of the H-Form was 284,000 +/- 25,000. The H-Form was dissociated into L-Form by incubation of cytosol at 37 degrees C. Triton X-100 (0.1%) and chlorpromazine (1.0 mM) also dissociated the H-Form into L-Form. Western blot analysis indicated that both forms contained the catalytic subunit. An increase in Mr 45,000 subunit coincided with the increase in cytidylyltransferase activity in L-Form, which resulted from the dissociated of H-Form. The L-Form was dependent on phospholipid for activity. The H-Form was active without lipid. Phosphatidylinositol was present in the H-Form isolated from Hep G2 cells. The phosphatidylinositol dispersed when the H-Form was dissociated into L-Form. Phosphatidylinositol and phosphatidylglycerol cause L-Form to aggregate into a form similar to H-Form. Phosphatidylcholine/oleic acid (1:1 molar ratio) and oleic acid also aggregated the L-Form. Phosphatidylcholine did not produce aggregation. We conclude that the H-Form is the active form of cytidylyltransferase in cytoplasm. The H-Form appears to be a lipoprotein consisting of an apoprotein (L-Form dimer of the Mr 45,000 subunit) complexed with lipids. A change in the relative distribution of H-Form and L-Form in cytosol would alter the cellular activity and thus may be important in the regulation of phosphatidylcholine synthesis.

Adenoma↗
PubMed1992

Changes in the expression of the tumor-associated antigen recognized by monoclonal antibody 44-3A6 in A549 cells due to calcium.

Although there is extensive data available on Ca2+ effects in normal tissues, comparatively little is known about its effects or regulation in tumor cells. The present studies were undertaken to investigate whether various extracellular calcium concentrations could modulate the expression of the tumor-associated antigen (TAA) recognized by monoclonal antibody (MAb) 44-3A6. It is highly expressed by the human lung adenocarcinoma cell line A549 and has been shown to be a 40-kD integral plasma membrane protein. Treatment of the A549 cell line with various concentrations of exogenous calcium showed a dose-dependent rise in the internal free calcium levels up to 2.4-2.9 mM (external calcium treatment). At higher concentrations, the internal calcium level showed a decline, indicating a higher calcium efflux. The calmodulin-dependent Ca(2+)-ATPase enzyme involved in calcium homeostasis was assayed under these same conditions. The enzyme activity increased with increasing external calcium concentrations showing a 5-fold increase in cells treated with 4.05 mM calcium. These data suggest that as the internal calcium approaches toxic levels, the Ca(2+)-regulated ATPase activity increases to reduce the calcium overload within the cell. Employing Western blot analysis and immunoperoxidase staining studies, this report shows that the antigen recognized by MAb 44-3A5 on A549 cells increased with an increase in calcium concentration. Evidence that this antigen is phosphorylated is presented using Western blot analysis of a radiolabeled antigen-enriched plasma membrane fraction. The previously reported subcellular localization, and now the phosphorylation and responsiveness to calcium by this TAA, gives it the properties predicted to be seen in a calcium 'pump-like' molecule. Thus, these studies support the hypothesis that this TAA may be important in intracellular calcium concentration control or that it is regulated via some calcium-mediated process.

Adenocarcinoma↗
PubMed1986

Cytoskeletal changes as an early event in hydrogen peroxide-induced cell injury: a study in A549 cells.

Hydrogen peroxide (H2O2) and other oxygen metabolites have been implicated in the pathogenesis of cell and tissue injury. The nature of the injury occurring in cells exposed to oxygen metabolites is unknown. A549 cells, derived from human lung carcinoma, were exposed to glucose-glucose oxidase or hydrogen peroxide in vitro. The distribution of actin and cytokeratin filaments, as well as 51chromium (51Cr) release and trypan blue dye exclusion were assessed. Both glucose-glucose oxidase and H2O2 resulted in changes which were time- and dose-dependent. Alterations in the cytoskeleton were detected by immunofluorescence microscopy at two hours, at which time the cells excluded trypan blue dye, while 51Cr release and trypan blue uptake first occurred at 8 h and required a five-fold greater concentration of glucose oxidase. The addition of catalase to glucose-glucose oxidase or H2O2, or inactivation of glucose oxidase by boiling, abrogated the injury. Therefore, one of the early targets of H2O2-induced cell injury may be the cytoskeleton.

Actins↗
PubMed1991

Inhibition of recovery from potentially lethal radiation damage in A549 cells by the K+/H+ ionophore nigericin.

A549 cells held for 4 hr in Hank's balanced salt solution, after 10 Gy irradiation, exhibit potentially lethal damage recovery (PLDR) which is dependent on extracellular pH (pHe). Recovery factors of 2.2 to 3.5 are observed when pHe is 6.40 to 7.30, but recovery factors of less than 1.0 are found when pHe is reduced to 6.20 or 6.00. The K+/H+ ionophore nigericin, when added to cells post-irradiation, inhibits PLDR in a pHe-dependent manner; it is increasingly more effective as pHe is reduced from 6.80 to 6.40. The presence of nigericin thus causes inhibition of PLDR at pHe's that normally promote recovery. The drug does not affect radiation response of A549 cells when present only during irradiation. Effects of low pHe buffer, with and without nigericin, on intracellular pH (pHi) and on ATP levels were examined in an effort to elucidate the mechanisms for inhibition of PLDR and enhancement of radiation response. Incubation of cells in pHe 6.00 buffer results in a slight decrease in pHi and does not induce a drop in ATP levels. In contrast, post-irradiation incubation of cells in pHe 6.40 buffer containing 2 microM nigericin causes an immediate and dramatic decrease in pHi, and a gradual loss of ATP to 30% of control levels by 4 hr. The data obtained so far suggest that a very slight lowering of pHi may influence post-irradiation holding recovery, and that the mechanisms by which pHe 6.00 buffer alone, or pHe 6.40 buffer containing nigericin, affect holding recovery are different.

Adenosine Triphosphate↗
PubMed1992

A novel pharmacological approach for paraquat poisoning in rat and A549 cell line using ambroxol, a lung surfactant synthesis inducer.

Paraquat (PQ) is a widely used herbicide that causes acute adult respiratory distress syndrome (ARDS) and chronic lung damage (diffuse fibrosis). One of the earliest biochemical effects induced by PQ is damage to type II pneumocytes with consequent depletion of surfactant. With the aim of counteracting the toxic effects of PQ, a series of investigations were performed into the possible protective effect of the drug ambroxol, which induces the synthesis of surfactant in lung alveolar type II cells. The number of survivors and survival time of rats treated ip with 35 mg PQ/kg was significantly increased by 3 days of ambroxol pretreatment and by ambroxol treatment 30 min or 2 hr after PQ. Total phospholipid content in lung and bronchoalveolar lavage fluid (BALF) was significantly reduced 30 hr after treatment with PQ alone. The association of ambroxol with PQ significantly antagonized this reduction. In BALF the ratio between palmitic acid and stearic acid concentrations was significantly lower in animals treated with PQ alone but was returned to normal by the association with ambroxol. The cell line A549, exposed in vitro to PQ concentrations from 0.5 x 10(-4) to 2 x 10(-3) M, showed a significant dose-dependent loss of viability. Cells pretreated with ambroxol (10 mg/ml) were more resistant to PQ and their viability started to decrease significantly only from a PQ concentration of 0.8 x 10(-3) M. Membrane microviscosity was measured on the same cells. Cells treated with PQ alone showed a reduction of membrane microviscosity, which was significantly counteracted by ambroxol pretreatment. The curves of modification of membrane microviscosity of cells treated with PQ and with ambroxol plus PQ paralleled those of cell viability, indicating that the stimulation of surfactant synthesis in vitro may be a prerequisite for counteracting some of the early effects of PQ.

Adenocarcinoma↗
PubMed1990

Diamide reduces cadmium accumulation by human lung carcinoma A549 cells.

Human lung carcinoma A549-T27 cells were used to determine the effect of diamide on cadmium accumulation. Treatment of the cells with diamide decreased their cellular glutathione content to 51.6 +/- 7% of control and significantly decreased their cadmium accumulation both as a function of time and as a function of Cd2+ concentration. Verapamil also decreased cadmium accumulation. Its effect compares well in magnitude with that which resulted from diamide treatment. No additive effect was observed when the cells were simultaneously treated with diamide and verapamil. The results suggest that a change in the GSH/GSSG ratio affects cadmium uptake. Further, calcium channels may be involved in cadmium uptake by A549-T27 cells in a fashion that is dependent on sulfhydryl status.

Azo Compounds↗
PubMed1992

An adventitious viral contaminant in commercially supplied A549 cells: identification of infectious bovine rhinotracheitis virus and its impact on diagnosis of infection in clinical specimens.

The isolation and identification of an adventitious viral agent, infectious bovine rhinotracheitis virus, in one lot of A549 cells from a commercial supplier is described in this report. The presence of infectious bovine rhinotracheitis virus in A549 cells was unexpected and has caused problems in the diagnosis of infections in clinical specimens in three laboratories.

Animals↗
PubMed1988

Inhibition of pentose cycle of A549 cells by 6-aminonicotinamide: consequences for aerobic and hypoxic radiation response and for radiosensitizer action.

Metabolism of glucose via the pentose cycle is a principal source of NADPH, an important cellular reducing species. Both aerobic and hypoxic irradiation stimulate the pentose cycle activity of A549 human lung carcinoma cells, which indicates that NADPH is utilized during irradiation, either as a direct hydrogen donor or as a cofactor for enzymatic repair of radiation damage. To evaluate the role of the pentose cycle in radiation response, we treated A549 cells with 6-aminonicotinamide (6-AN), which blocks the oxidative limb of this pathway in some cell lines. We found 6-AN to be a very effective inhibitor of pentose cycle activity, as indicated both by accumulation of 6-phosphogluconate in A549 cells and by the inability of nitrofurazone or peroxide to stimulate release of 14CO2 from 14C-1-labeled glucose after 6-AN treatment. Effects of 6-AN were time and concentration dependent; it caused partial inhibition of glycolysis but had no effect on respiratory rate or on intracellular glutathione levels. Effects of 6-AN on radiation response were examined under two conditions: 1) after treatment with 0.3 mM drug for 5 hours, which inhibited pentose cycle activity by 50%, and 2) after treatment for 15 hours, which completely inhibited pentose cycle activity. Neither treatment affected aerobic radiation response, but both increased hypoxic sensitivity to a similar extent, with the oxygen enhancement ratio reduced from 3.0 to 2.0 at a 0.05 surviving fraction. Treatment of A549 cells with 6-AN caused an increase in hypoxic cell radiosensitization by misonidazole, but effects of the combined agents were not more than additive.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Aminonicotinamide↗
PubMed1989

Enhanced cadmium cytotoxicity in A549 cells with reduced glutathione levels is due to neither enhanced cadmium accumulation nor reduced metallothionein synthesis.

Glutathione (GSH) depletion sensitizes human lung carcinoma (A549-T27) cells to the cytotoxic effects of Cd++. The effects of GSH depletion on Cd++ accumulation and Cd++-induced metallothionein (MT) content were investigated to determine the possible role of these Cd++ responses in the sensitization process. Cellular GSH was depleted to 20% to 25% of control levels with buthionine sulfoximine (BSO), or diethyl maleate (DEM), respectively. Neither treatment significantly affected Cd++-induced accumulation of exogenous 35s-cysteine into intracellular MT in a dose-dependent fashion. The results indicate that neither enhanced Cd++ accumulation nor reduced MT synthesis plays a primary role in affecting enhanced Cd++ cytotoxicity in A549 cells with reduced GSH levels. Although BSO inhibition of GSH synthesis enhanced MT synthesis, it sensitized the cells to Cd++, which suggests an additive effect of GSH and MT in cadmium cytoprotection. This observation also raises the possibility that intracellular cysteine levels limit Cd++-induced MT accumulation rates.

Buthionine Sulfoximine↗
PubMed1992

Okadaic acid strongly increases gene transcription, mRNA and protein level for the urokinase receptor in human A549 cells.

The specific phosphatase inhibitor, okadaic acid, increases the level of mRNA for the receptor for urokinase-type plasminogen activator (u-PAR) in 8 out of 13 human cell lines. The strongest increase (90-fold) was observed in A549 lung carcinoma cells, in which it was partly traced back to an increased transcription of the u-PAR gene. There was a parallel but less pronounced increase in the u-PAR protein level. These findings indicate that u-PAR gene transcription is regulated by one or more factors that are constitutively phosphorylated and are dephosphorylated by okadaic acid-sensitive phosphatases. A lack of additivity of u-PAR induction by okadaic acid and by the protein kinase C activator, PMA, in the A549 cells suggests that the regulatory factors affected by okadaic acid are phosphorylated by protein kinase C.

Blotting, Northern↗
PubMed1986

Growth experiment of Hantaan virus in A549 cells: an attempt to improve the immunofluorescent antibody technique for hemorrhagic fever with renal syndrome.

An assay method for the infectivity of Hantaan virus, a causative agent of HFRS (hemorrhagic fever with renal syndrome), was developed by the use of IFA (immunofluorescent antibody technique). With the aid of this method, the growth characteristics of Hantaan virus, 76-118 strain, were followed in A549 cells. At a maximal MOI (multiplicity of infection) of 1.6 VAIU (viral antigen-inducing units) per cell, the conventionally available value, plateau level potencies of the viral antigen and virus infectivity were attained at eight and ten days postinfection, respectively, and most of the infective virus produced accumulated in the culture fluids of infected cells. When infections were defined with MOI values in terms of VAIU per cell, development of the viral antigen was highly consistent and followed a given pattern of kinetics. Based on these findings, a protocol for preparation of the viral antigen in IFA was presented, wherein spot culture and FBS treatment were emphasized as effective procedures to minimize non-specific staining.

Animals↗
PubMed1989

Detection of herpes simplex virus in clinical specimens using a DNA probe after centrifugal inoculation of A549 cells.

Two methods for detection of herpes simplex virus (HSV) in 216 clinical specimens were compared: (a) 24-well plate centrifugation using A-549 cells followed by nucleic acid hybridization (Ortho Diagnostic Systems, Inc., Raritan, NJ) after incubation for 16 to 18 h, and (b) conventional tube cell culture using A-549 cells. HSV was identified by conventional tube cell culture in 44 of 216 specimens (20%) and in 36 specimens (17%) by the centrifugation-hybridization method (P less than 0.01). HSV was recovered by tissue culture from all specimens positive by centrifugation-hybridization. The sensitivity, specificity, and positive and negative predictive values of the centrifugation-hybridization technique for detection of HSV in clinical specimens were 82, 100, 100, and 96%, respectively. Centrifugal inoculation of A549 cells in 24-well plates followed by nucleic acid hybridization after overnight incubation should not replace conventional tube cell culture for detection of HSV in clinical specimens.

Cells, Cultured↗
PubMed1986

The effect of pH on potentially lethal damage recovery in A549 cells.

The radiation sensitivity and potentially lethal damage recovery (PLDR) capacity of A549 human lung carcinoma cells have been studied. For unfed monolayer cultures, radiation sensitivity was greater in plateau phase than in log phase of growth. PLDR was observed when plateau-phase cells were held in their own spent medium postirradiation, such that the dose-response curve with 24 h holding was similar to that for log-phase cells plated immediately after irradiation. The high PLDR capacity of A549 plateau-phase cells (recovery factor between 40 and 70 for 24 h holding after 10 Gy) was reduced 10-fold or more by alkalinizing the pH of the spent medium immediately after irradiation from a value of 6.5 +/- 0.1 to a value of 7.6. Medium alkalinization resulted in an increase in the rate of glycolysis, with subsequent reacidification to a pH of 7.3 within 2 h of the pH adjustment. No change in cell cycle distribution was observed in the plateau-phase cultures up to 32 h after change of medium pH, and no increase in cell density was found after 48 h. A slight increase in the rate of incorporation of radiolabeled thymidine into acid-precipitable material was observed at 4 and 24 h after alkalinization of the medium. While it is not possible at present to define a mechanism for this pH effect, our results demonstrate that, at least for this cell line, variables such as medium pH and glucose concentration can profoundly influence the observation of PLDR.

Cell Line↗
PubMed1992

The differential susceptibility of A427 and A549 cell lines to the growth-inhibitory effects of ET-18-OCH3 does not correlate with the relative effects of the alkyl-lysophospholipid on the incorporation of fatty acids into cellular phospholipids.

Proliferation of A427, a lung cancer cell line, was significantly decreased 10 h after incubation with 5 micrograms/ml 1-O-octadecyl-2-O-methylglycero-3-phosphocholine (ET-18-OCH3) while the proliferation of A549, another lung cancer cell line, was unaffected until 15 h after incubation with the alkyl-lysophospholipid (ALP). The relative sensitivity of cells to the antiproliferative effect of ET-18-OCH3 has been postulated to be due to the degree of inhibition of cellular acylation processes. We therefore investigated the effect of 5 micrograms/ml ET-18-OCH3 on the incorporation of fatty acids for up to 12 h, into A427 and A549 phospholipids. Significant changes observed in the incorporation of fatty acids into A427 phospholipids by the ALP were a decreased incorporation of oleic acid into PC after 8 h, an increased incorporation of linoleic acid into PE after 12 h, decreased incorporation of arachidonate into PE after 3 h, and increased incorporation into PA after 5 h. Although the above changes affected the distribution of newly esterified fatty acids in the phospholipids, there was no effect on the total quantity of label incorporated in the phospholipid fraction between the experimental and control cells after 12 h. Incubation of A549 cells with ET-18-OCH3 resulted in decreased esterification of oleic acid into PC, SM, and LPC after 5 h; decreased incorporation of linoleic into PE after 12 h; and a decreased incorporation of arachidonate into SM after 1.5 h. After 12 h incubation with ET-18-OCH3, changes in the distribution of radiolabeled fatty acids were observed in the quantitatively minor phospholipids, SM and LPC. A 20% decrease in the quantity of oleic acid incorporated into the phospholipids was observed in cells incubated with the ALP; however, no differences were observed in the quantity of linoleic or arachidonic acid incorporated into the phospholipids. The lack of common effects of the ALP on the incorporation of fatty acids into A427 and A549 phospholipids, coupled with the absence of changes that were more severe or manifested earlier in the more sensitive A427 cell line, suggests that the effect of ET-18-OCH3 on the acylation processes depends on the cell type and the fatty acid species and is unlikely to be responsible for the relative sensitivities of the cells to the compound. Radiolabeled ET-18-OCH3 was used to examine the correlation between the amount of the compound accumulated in A427, A549, MCF7, T84, and LS174T cells and the relative susceptibilities of the cells to the ALP.(ABSTRACT TRUNCATED AT 400 WORDS)

Acylation↗
PubMed1991

Differential regulation of the expression of transforming growth factor-beta s 1 and 2 by retinoic acid, epidermal growth factor, and dexamethasone in NRK-49F and A549 cells.

Although most biological activities of transforming growth factor-beta s 1 and 2 (TGF-beta 1 and TGF-beta 2) examined in vitro are similar or identical, recent studies suggest that each of these factors may be independently regulated in vivo. In this study we have used highly sensitive and specific sandwich enzyme-linked immunosorbent assays for TGF-beta 1 and TGF-beta 2 to examine the effects of a variety of treatments on expression of these two TGF-beta isoforms. We show that epidermal growth factor (EGF) induces secretion of TGF-beta 1 and not TGF-beta 2, whereas retinoic acid (RA) induces secretion of TGF-beta 2 and not TGF-beta 1 in NRK-49F normal rat kidney fibroblasts and A549 human lung carcinoma cells. Moreover, treatment with EGF diminishes the levels of TGF-beta 2, while RA decreases the levels of TGF-beta 1 in both cell lines. Dexamethasone (Dex), on the other hand, inhibits the secretion of both TGF-beta 1 and TGF-beta 2 in A549 cells, while selectively inhibiting TGF-beta 1 secretion in NRK-49F cells. The interactive effects of EGF, RA, and Dex on the production of TGF-beta 1 and TGF-beta 2, which were studied on NRK-49F cells, demonstrate that EGF blocks the induction of TGF-beta 2 mRNA and peptide by RA, while Dex inhibits the induction of TGF-beta 1 mRNA and peptide by EGF. These results demonstrate that RA, EGF and Dex are each unique, differential, and interactive regulators of the expression of TGF-beta s 1 and 2.

Animals↗
PubMed1990

Cellular cadmium responses in subpopulations T20 and T27 of human lung carcinoma A549 cells.

Subpopulations T20 and T27, cloned from the human lung carcinoma line A549, differ significantly in their Cd2+ cytotoxic response. T27 has an LC50 of 31 microM Cd2+ and a cytotoxic response threshold of 5 microM Cd2+, whereas the T20s LC50 is 15 microM Cd2+ and there is no observed threshold for cytotoxicity. Cadmium-induced metallothionein (MT) synthesis, cadmium accumulation, glutathione (GSH) content, and Cd2(+)-induced changes in GSH content were studied in T20 and T27 in an attempt to determine the mechanism(s) causing differential cytotoxic response. MT synthesis measured by following Cd2(+)-induced [35S] incorporation into MT was found not to differ between T20 and T27. There is, however, a difference in Cd2+ accumulation between the two subclones. T20 and T27 cells were exposed to 5 microM Cd2+ for different times or to different concentrations of Cd2+ for 8 h. The T27 subline, which is the more Cd2+ resistant, was found to accumulate significantly more Cd2(+)-both as a function of time exposed to Cd2+ and as a function of Cd2+ concentration. The two subpopulations were found to have comparable initial GSH contents, but showed different Cd2(+)-induced changes in [GSH] when the cells were exposed to 5 microM Cd2+. T27 cells maintained their GSH content following Cd2+ exposure but T20 cells showed a Cd2(+)-induced decrease in GSH content. The results indicate that the difference in Cd2+ cytotoxic response between A549--T20 and A549--T27 cells is not attributable to alterations in MT synthesis nor to a difference in initial GSH content. Relative Cd2+ cytotoxicity also does not in these cells correlate with relative Cd2+ accumulation. The fact that T27 cells accumulate more Cd2+ and yet are more Cd2+ resistant than T20 cells suggests that T27 cells have a much more effective non-MT mechanism to handle intracellular Cd2+. This may involve different GSH metabolism and/or yet undefined molecular factors.

Cadmium↗
PubMed1992

Transport of choline by plasma membrane vesicles from lung-derived epithelial cells.

A549 cells, a lung epithelium-derived cell line, were used as a model system to study choline transport by granular pneumocytes. Intact cells accumulated free choline against a concentration gradient by a low-affinity transport system with kinetic characteristics similar to that previously described for granular pneumocytes (Am. J. Respir. Cell Mol. Biol. 1: 455, 1989). Membrane vesicles prepared from these cells showed a 10-fold enrichment in plasma membrane marker enzymes with a vesicular H2O space of 5.7 +/- 0.05 (SE) microliters/mg protein. Vesicles showed a time- and concentration-dependent uptake of free [3H]choline in Na(+)-free medium. With 5 microM choline, choline uptake reached an apparent steady-state concentration gradient (inside/outside) of 50. 3H that was membrane associated ("bound" choline) represented approximately 5% of total uptake. In the presence of an initial gradient of NaCl, choline uptake showed an overshoot with a plateau value similar to Na(+)-free conditions; a similar effect was observed for plasma membrane vesicles from rat lung type 2 epithelial cells. The steady-state uptake of choline was inhibited at low pH (6.5) and by the presence of valinomycin or carbonyl cyanide p-tri-fluoromethoxyphenylhydrazone and was abolished when both were present. These results show that plasma membrane vesicles from A549 cells accumulate choline by binding to the membranes and by Na(+)-dependent and -independent transport mechanisms, the latter apparently reflecting a transmembrane proton gradient.

Animals↗