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B M Woloski

Publications and source records attributed to B M Woloski.

16 recordsLinked to original sources
PubMed1990

Stimulation of release of Gal beta 1-4GlcNAc alpha 2-6 sialyltransferase from the FAZA hepatoma cell line by dexamethasone and phorbol ester.

1. Gal beta 1-4GlcNAc alpha 2-6 sialyltransferase was assayed in FAZA hepatoma cells and the cell culture medium following growth of cells in presence of dexamethasone and phorbol ester. 2. There was about a seven-fold increase in sialyltransferase activities in cells and medium in presence of dexamethasone with the maximum effect occurring at 10(-6)-10(-7) M dexamethasone. 3. The presence of 10(-6) M phorbol ester in the culture medium increased sialyltransferase activities in cells and medium by ca 40% over the values found with dexamethasone alone. 4. The use of the FAZA hepatoma cell line for studies on sialyltransferase is compared with the primary hepatocyte system reported on earlier (Woloski et al., 1986).

Animals↗
PubMed1987

Isolation of hepatocyte stimulating factor from human monocytes.

Hepatocyte stimulating factor is a monocyte derived protein which regulates hepatic plasma protein synthesis. Human hepatocyte stimulating factor was purified to apparent homogeneity from adherent peripheral blood monocytes by using ion exchange, gel permeation and reversed phase chromatography. Electrophoretic analysis showed that it has a Mr of 28,000 daltons and an isoelectric point of 5.4. Biological assays specific for hepatocyte stimulating factor and interleukin-1 showed that they are distinct and have independent biological effects.

Animals↗
PubMed1987

Rat corticotropin, insulin and thyroid hormone levels during the acute phase response to inflammation.

Circulating levels of corticotropin, thyroid hormones and insulin were measured in rats at various times after turpentine-induced inflammation. Corticotropin increased rapidly showing a biphasic response with a four-fold increase at about 6-8 hr after inflammation and a 10-fold increase at 10 hr after inflammation. The response of insulin to inflammation was slower than corticotropin and the magnitude of the increase was smaller. Insulin increased by three-fold at 20 hr after inflammation. Thyroid hormone levels were depressed by turpentine inflammation. Levels fell after 4 hr and remained at low levels throughout. Administration of a cytokine preparation to rats also caused depressed thyroxine levels at short intervals after administration. However, levels increased at longer intervals after administration. This suggests that, like corticotropin and insulin, thyroid hormone levels could be under the control of immunotransmitters during the acute phase response.

Adrenocorticotropic Hormone↗
PubMed1987

The acute phase response to inflammation: the role of monokines in changes in liver glycoproteins and enzymes of glycoprotein metabolism.

The role of monocyte derived factors in the acute phase response to inflammation is discussed. The kinetics of response of alpha 1-acid glycoprotein, sialyltransferase and albumin to a rat monokine preparation is described. There was an increase in synthesis of alpha 1-acid glycoprotein and sialyltransferase and a decrease in albumin synthesis following administration. However, the kinetics of response of sialyltransferase to the monokine was much slower than was found for the other two proteins. The possibility that sialyltransferase responds to a different monokine compared to the other acute phase proteins is discussed.

Acute-Phase Reaction↗
PubMed1986

Studies on the effect of the hepatocyte-stimulating factor on galactose-beta 1----4-N-acetylglucosamine alpha 2----6-sialyltransferase in cultured hepatocytes.

Rat hepatic Gal beta 1----4GlcNAc alpha 2----6 sialyltransferase is released into the blood at elevated levels following an inflammatory challenge: this is a typical response of the group of plasma proteins known as acute-phase reactants. In the present study, primary cultures of liver parenchymal cells are used to demonstrate that the same hepatic cell type that produces plasma proteins such as fibrinogen also produces and releases sialyltransferase. Hepatic production of sialyltransferase is stimulated by a major regulator of hepatic acute-phase reactant production, the hepatocyte-stimulating factor (HSF), while another monokine, interleukin-1, does not affect hepatocyte sialyltransferase production. The maximum increase in sialyltransferase occurs 48 h after exposure to HSF which is considerably later than the fibrinogen response. The sialyltransferase that is stimulated by HSF is the Gal beta 1----4GlcNAc alpha 2----6 isozyme.

Animals↗
PubMed1985

Corticotropin-releasing activity of monokines.

Hepatocyte-stimulating factor and interleukin-1 are proteins produced by monocytes in response to inflammatory challenge. Neither of these monokines had direct effects on steroid production by cultured adrenocortical cells. Both monokines stimulated pituitary cells (AtT-20) to release adrenocorticotropic hormone; interleukin-1 was equipotent with a combination of corticotropin-releasing factor and arginine vasopressin, and hepatocyte-stimulating factor was at least three times as effective. The synthetic glucocorticoid, dexamethasone, inhibited production of hepatocyte-stimulating factor by cultured monocytes. These results indicate an axis between monocytes and pituitary and adrenocortical cells which may play a role in regulating host defense.

Adrenal Glands↗
PubMed1985

Studies of monokines as mediators of the acute phase response: effects on sialyltransferase, albumin, alpha 1-acid glycoprotein and beta-N-acetylhexosaminidase.

Rat peritoneal leukocytes (PEC) were fractionated on Percoll gradients to prepare populations of monocytes/lymphocytes and polymorphonuclear leukocytes; adherent (monocyte enriched) and non-adherent (lymphocytes/polymorphonuclear leukocytes) cells were also isolated from PEC. Cytokines were prepared from PEC and subfractions and injected into rats to induce the acute phase reactants serum alpha 1-acid glycoprotein and sialyltransferase; negative acute phase parameters serum albumin and liver hexosaminidase were also assayed. Monocyte derived cytokines (monokines) mimicked the acute phase response of all four parameters in vivo. The sialyltransferase isoenzyme that responded to monokine was identified as the Gal beta 1----4GlcNAc alpha 2----6 isoenzyme.

Animals↗
PubMed1985

Identification and partial characterization of hepatocyte-stimulating factor from leukemia cell lines: comparison with interleukin 1.

Leukemia cell lines of the monocytic series (HL-60, U-937, and P388D1) produce a hepatocyte-stimulating factor (HSF) following induction of differentiation with phorbol diester. In 24-72 hr, these leukemia cells produce 2-30% the amount of HSF as human peripheral blood monocytes. Cells of the series at earlier stages of differentiation produced greater amounts of HSF. Fractionation of the medium from each cell type by HPLC reveals much of the HSF activity in the 25- to 30-kilodalton range. Under the same culture conditions, interleukin 1 is produced; however, its bioactivity is in the 7- to 15-kilodalton range. Neither monokine shows reciprocal bioactivity. Superinducing culture conditions that greatly increase interleukin 1 production completely eliminate HSF production, suggesting that there is different stability of the mRNA coding for each protein or that there are different temporal events important to the induction of synthesis of these proteins.

Animals↗
PubMed1985

The effects of hepatocyte stimulating factor on fibrinogen biosynthesis in hepatocyte monolayers.

The biosynthesis of fibrinogen increased at least eightfold in primary hepatocytes when incubated in the presence of monocyte/macrophage-derived hepatocyte stimulating factor (HSF). The large increase in fibrinogen production is due to increased availability of the mRNAs for the protein since cytodot analysis of cellular RNA showed a 10-12-fold increase in each of the fibrinogen mRNAs. Pulse-chase experiments showed that the time for fibrinogen synthesis, assembly, and secretion was 40-50 min for both control and stimulating conditions. This indicates that the increased production was due principally to the presence of greater amounts of fibrinogen mRNA rather than translation or secretion-specific events. Three lines of evidence indicate that the increase in fibrinogen production was due to HSF effects on transcription: (a) analysis of cytoplasmic levels of each of the fibrinogen mRNAs showed that all three increased at the same rate and to the same extent, demonstrating that HSF affects the three gene products coordinately; (b) Northern gel analysis of cytoplasmic RNA isolated after very brief exposures to HSF showed increases in a large molecular weight fibrinogen RNA precursor; and (c) actinomycin D blocked the HSF-stimulated increase in fibrinogen mRNA species. Furthermore, experiments in which protein synthesis was inhibited by cycloheximide failed to inhibit the increase in fibrinogen mRNAs, indicating new protein synthesis is not required for the HSF stimulation of fibrinogen mRNA. These results are consistent with our hypothesis that HSF is exerting its control of fibrinogen at the level of gene transcription.

Animals↗
PubMed1984

Studies of the effect of experimental inflammation on rat liver nucleotide sugar pools.

The effect of experimental inflammation on levels of nucleotide sugars was studied in rat liver. There was an increase of about 2-fold in the levels of UDP-N-acetylhexosamines and GDP-Man at 8 and 4 hr after inflammation, respectively. At 48 hr after inflammation GDP-Man had returned close to control values, but UDP-N-acetylhexosamines were still about 50% above controls. There was a 30% reduction in CMP-NeuAc and UDP-Gal at 8-12 hr after inflammation before increasing to slightly above controls at 16-48 hr after inflammation. Inflammation resulted in an increase in activities of glucosamine-6-phosphate synthase and UDP-GlcNAc-2'-epimerase to about twice control activities at 24 and 8 hr after inflammation, respectively, before declining; CMP-NeuAc synthase activities did not show large changes following inflammation.

Acetylgalactosamine↗
PubMed1983

Studies on the effect of inflammation on rat liver and serum sialyltransferase. Evidence that inflammation causes release of Gal beta 1 leads to 4GlcNAc alpha 2 leads to 6 sialyltransferase from liver.

Turpentine induced inflammation has been shown to elevate liver sialyl- and galactosyltransferase activities (Turchen, B., Jamieson, J.C., Huebner, E., and van Caeseele, L. (1977) Can. J. Zool. 55, 1567-1571; Lombart, C., Sturgess, J., and Schachter, H. (1980) Biochem. Biophys. Acta 629, 1-12). We now report that serum sialyl-, but not galactosyltransferase activities are significantly elevated in turpentine inflammation. A liver slice system is used to demonstrate that liver releases large amounts of sialyltransferase activity into medium after inflammation, whereas only a low level of galactosyltransferase activity is released. Studies with rat and human asialo-alpha 1-acid glycoprotein as acceptors, coupled with the use of lactose to confirm the nature of the linkages formed, showed that Gal beta 1 leads to 4GlcNAc alpha 2 leads to 6 sialyltransferase is released from liver in turpentine inflammation and is mainly responsible for the elevated sialyltransferase activity found in serum. The alpha 2 leads to 6 sialyltransferase is exhibiting the properties of a typical acute phase reactant.

Animals↗
PubMed1983

Studies on rat cytokines as mediators of the acute phase response.

A cytokine preparation from rat peritoneal exudate cells was studied. The preparation was pronase sensitive and heat labile, but was insensitive to trypsin treatment. Administration to rats resulted in elevated serum levels of alpha 1-acid glycoprotein, sialyltransferase activities and cortisol, but depressed serum albumin levels; in addition, hepatic sialyltransferase activities were increased and hepatic beta-galactosidase and beta-N-acetylhexosaminidase activities were depressed.

Animals↗
PubMed1983

Glycoprotein biosynthesis during the acute-phase response to inflammation.

Inflammation results in an increase in the levels of a variety of glycoproteins in serum. The glycoproteins that respond in this way are usually referred to as acute-phase reactants. Studies on the acute-phase response of rat alpha 1-acid glycoprotein showed that there was an increase in the liver levels of this glycoprotein at 12 h after turpentine inflammation. This was followed by increased serum levels at 48-72 h after inflammation, suggesting a precursor-product relationship between liver and serum alpha 1-acid glycoprotein. Incorporation studies coupled with measurements of synthesis rates of alpha 1-acid glycoprotein showed that increased synthesis was responsible for the acute-phase response of this protein to inflammation. These studies also showed that albumin was a negative acute-phase reactant. The acute-phase response of alpha 1-acid glycoprotein was accompanied by increased liver pools of UDP-N-acetylglucosamine (UDP-GlcNAc) and UDP-N-acetylgalactosamine (UDP-GalNAc) and increased liver activities of glucosamine-6-phosphate synthase and UDP-GlcNAc 2-epimerase. Activities of galactosyl and sialyl transferases in liver were also elevated and serum sialyl transferase was increased substantially in inflammation, suggesting that it may also be an acute-phase reactant. Liver activities of beta-N-acetylhexosaminidase and beta-galactosidase declined by about 50% at 24 h after inflammation; there was evidence that serum levels of these enzymes increased at 24-72 h after inflammation, suggesting that the lysosomal glycosidases may be released from liver during inflammation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗