Studies on the stimulation of dolichol-mediated glycosylation by dexamethasone in HeLa cells

Ramachandran, Chittoor K.; Gray, Sue; Melnykovych, George

doi:10.1042/bj2080047

Cited by 9 publications

(3 citation statements)

References 25 publications

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“…A stimulatory effect of dexamethasone on the synthesis of certain classes of secretory glycoproteins has been reported by Baumann et al (1983) in hepatoma tissue-culture cells and in primary hepatocyte culture. Furthermore, increased formation of dolichol-linked sugar derivatives by dexamethasone has been shown in HeLa cells (Ramachandran et al, 1982). The results given in the present paper are complementary to those observations.…”

supporting

confidence: 81%

Effect of dexamethasone on mannolipid synthesis by hepatocytes prepared from control and inflamed rats

Sarkar¹,

Mookerjea²

1984

Biochemical Journal

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Hepatocytes were prepared from control and inflamed rats. Mannose incorporation into dolichol monophosphate mannose in homogenate and microsomal fraction of the hepatocytes was increased 2-fold over the controls 24h after induction of inflammation by turpentine injection. Incubation of hepatocytes from both control and inflamed rats with 0. 1-O0Mm-dexamethasone produced a 1.5-fold increase of dolichol phosphate mannose formation, whereas, 100 MM-dexamethasone decreased its formation. The increase in the ratio of dolichol phosphate mannose formation in inflamed over controls was virtually eliminated when the cell homogenate assay mixtures included 30nmol of exogenous dolichol phosphate. This supports the earlier suggestion that the increase in the enzyme activity in inflammation could be due to higher concentrations of endogenous dolichol phosphate [Coolbear & Mookerjea (1981) J. Biol. Chem. 256, 4529-4535]. In contrast, the increase in the ratio of dolichol phosphate mannose formation between dexamethasone-treated and untreated hepatocytes remained unchanged when increasing concentrations of exogenous dolichol phosphate were added to the assays. This suggests that the increase in glycosylation of dolichol phosphate in dexamethasone-treated hepatocytes is probably due to the increased mannosyltransferase activity, rather than due to higher concentrations of endogenous dolichol phosphate in these cells.

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supporting

confidence: 81%

Effect of dexamethasone on mannolipid synthesis by hepatocytes prepared from control and inflamed rats

Sarkar¹,

Mookerjea²

1984

Biochemical Journal

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“…It appears that, like compactin and (-)-hydroxycitrate, dexamethasone very rapidly gives rise to opposing changes in these activities, whereas the rate of fatty acid synthesis was unchanged ( Table 1). In contrast, in HeLa cells, there is a lag period of 12-16h before the effect of dexamethasone on HMG-CoA reductase activity becomes apparent (Cavenee & Melnykovych, 1977;Ramachandran et al, 1982).…”

Section: Resultsmentioning

confidence: 99%

The role of substrate supply in the regulation of cholesterol biosynthesis in rat hepatocytes

Pullinger¹,

Gibbons²

1983

Biochemical Journal

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1. Compactin, (-)-hydroxycitrate and dexamethasone gave rise to a decrease in the rate of cholesterol production in hepatocytes from fed rats by interfering with the flow of substrate into the sterol biosynthetic pathway. The cells responded to the deficit of biosynthetic sterol by increasing the activity of hydroxymethylglutaryl-CoA reductase (HMG-CoA reductase). 2. Compactin and (-)-hydroxycitrate gave similar results in hepatocytes from rats starved for 24 h but in this case dexamethasone had no significant effect. 3. Exogenous oleate interferes with the production of carbohydrate-derived acetyl-CoA and also gives rise initially to opposing effects on the rate of sterol synthesis and HMG-CoA reductase activity. Over a longer period, however, oleate itself was capable of replacing carbohydrate as the major source of carbon for sterol synthesis. 4. The increase in HMG-CoA reductase activity observed when liver cells were incubated in the presence of compactin, (-)-hydroxycitrate or oleate could be partially reversed by the simultaneous presence of glucagon. 5. Under some physiological conditions, a deficiency of biosynthetic cholesterol or of a related precursor may lead to an increase in the activity of HMG-CoA reductase.

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“…Since our early studies have demonstrated a glucocorticoid-stimulated increase in alkaline phosphatase (Melnykovych, 19621, an enzyme which could be involved in the degradation of both dolichol phosphate and retinol phosphate, a study of the effects of both glucocorticoids and vitamin A compounds on the levels of activity of alkaline phosphatase seemed indicated. It is noteworthy that glucocorticoids, in addition to their effects on alkaline phosphatase, also increase the levels of cellular dolichols and dolichylmannolipids (Ramachandran et al, 1981, Ramachandran et al, 1982.…”

mentioning

confidence: 99%

Synergistic stimulation of alkaline phosphatase activity in bovine aortic endothelial cells grown in the presence of retinoids and glucocorticoids

Adams

Melnykovych

1985

Journal Cellular Physiology

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Low concentrations of retinol (10 nM-10 microM) and dexamethasone (0.1 nM-1.0 microM) elevated activity of alkaline phosphatase (E.C. 3.1.3.1) in bovine endothelial cells in culture. The effect was apparent after 48 hr of growth in the presence of either of the two compounds, prior to any growth stimulatory effects. A synergistic stimulation of alkaline phosphatase was achieved in the presence of both retinol and dexamethasone implying different mechanisms of induction. Retinoic acid and retinyl acetate also elevated alkaline phosphatase but the retinol analogue reduced in the side chain (perhydroretinol) was inactive. The ability of steroids to elevate alkaline phosphatase activity was associated with the structure commonly required for glucocorticoid activity; however, competitors for the steroid receptor binding failed to prevent the elevation by dexamethasone or the synergism in the presence of retinol and dexamethasone.

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Studies on the stimulation of dolichol-mediated glycosylation by dexamethasone in HeLa cells

Cited by 9 publications

References 25 publications

Effect of dexamethasone on mannolipid synthesis by hepatocytes prepared from control and inflamed rats

Effect of dexamethasone on mannolipid synthesis by hepatocytes prepared from control and inflamed rats

The role of substrate supply in the regulation of cholesterol biosynthesis in rat hepatocytes

Synergistic stimulation of alkaline phosphatase activity in bovine aortic endothelial cells grown in the presence of retinoids and glucocorticoids

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