14 results on '"Milovic A"'
Search Results
2. Butyrate and the cytokine-induced α1-proteinase inhibitor release in intestinal epithelial cells
- Author
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Faust, D., Hormann, S., FriedrichSander, M., Milovic, V., and Stein, J.
- Published
- 2001
Catalog
3. Nonsteroidal anti‐inflammatory drugs stimulate spermidine/spermine acetyltransferase and deplete polyamine content in colon cancer cells
- Author
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Turchanowa, L., Dauletbaev, N., Milovic, V., and Stein, J.
- Published
- 2001
4. Influence of physical exercise on polyamine synthesis in the rat skeletal muscle
- Author
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Turchanowa, L., Rogozkin, V. A., Milovic, V., Feldkoren, B. I., Caspary, W. F., and Stein, J.
- Published
- 2000
5. Effects of deoxycholate on human colon cancer cells: apoptosis or proliferation
- Author
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Jürgen Stein, Vladan Milovic, Wolfgang F. Caspary, D Faust, and I. C. Teller
- Subjects
medicine.medical_specialty ,Programmed cell death ,Bile acid ,Colorectal cancer ,medicine.drug_class ,Cell growth ,Clinical Biochemistry ,Deoxycholic acid ,General Medicine ,Biology ,medicine.disease ,Biochemistry ,Malignant transformation ,chemistry.chemical_compound ,Endocrinology ,chemistry ,Apoptosis ,Caco-2 ,Internal medicine ,medicine ,Cancer research - Abstract
Background Deoxycholic acid has long been attributed as a tumour promoter in the colon. It exerts its growth-related actions in a phorbol ester-like manner, by stimulating protein kinase C. The aim of this study was to investigate the effect of deoxycholic acid on proliferation and apoptosis in the colon, by exposing colon cancer cells to it in increasing concentrations. Methods Human colon cancer cells (Caco-2 and HT-29) were treated with deoxycholate or its two structural isomers, 3-beta-12-alpha-dihydroxy-5-beta-cholan-24-oic acid and 3alpha-12-beta-dihydroxy-5-beta-cholan-24-oic acid. Proliferation was evaluated by cell counting, and apoptosis by estimating percentage cell survival and assessment of nuclear morphology. Results Within the concentration range of up to 20 aeM, deoxycholate stimulated growth of both human colon cancer cell lines. Its growth-promoting effect was abolished after inhibition of protein kinase C. At concentrations above 100 aeM, deoxycholate induced apoptosis in both cell lines. Epimers of deoxycholate were significantly less potent in stimulating growth. Conclusion Low-dose deoxycholate stimulates colon cancer cell proliferation while > 100 aemol L -1 of this secondary bile acid induces apoptosis in colon cancer cells. Deoxycholate might promote the likelihood of malignant transformation by increasing epithelial cell turnover in the colon. more...
- Published
- 2002
- Full Text
- View/download PDF
6. Butyrate and the cytokine-induced α1-proteinase inhibitor release in intestinal epithelial cells
- Author
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Vladan Milovic, M Friedrich-Sander, Jürgen Stein, D Faust, and S. Hormann
- Subjects
medicine.medical_specialty ,medicine.diagnostic_test ,medicine.medical_treatment ,Clinical Biochemistry ,Inflammation ,General Medicine ,Butyrate ,Biology ,Biochemistry ,Molecular biology ,Proinflammatory cytokine ,Endocrinology ,Immune system ,Cytokine ,Western blot ,Caco-2 ,Cell culture ,Internal medicine ,medicine ,medicine.symptom - Abstract
Background Alpha1-proteinase inhibitor (alpha1-PI), an anti-inflammatory protein thought to play a role in the intestinal inflammation, is synthesised by and released from the intestinal epithelial cells. IL-1beta is a key proinflammatory cytokine in the abnormal immune response that occurs in inflammatory bowel disease. Butyrate is a normal luminal constituent in the colon, known to be of benefit in preventing inflammatory bowel disease. Direct modes of action of butyrate in intestinal inflammation have been poorly studied so far. The aim of this study was to investigate the effects of butyrate on cytokine-mediated alpha1-PI release in intestinal epithelial cells. Methods Differentiated Caco-2 cells were incubated with IL-1beta in the presence or absence of 2 mM butyrate. Alpha1-PI expression in the cells was evaluated by Western blot analysis and alpha1-PI release by ELISA. Results Treatment with butyrate alone had no effect on alpha1-PI expression in differentiated Caco-2 cells. However, treatment of the cells with 2 mM butyrate significantly reduced the alpha1-PI level in IL-1beta-treated cells. In the cell culture medium, the presence of butyrate impaired the IL-1beta-induced alpha1-PI release to 17-35%. The treatment induced no change in the number of detached cells or the percentage of viable cells. Conclusion Our data show that butyrate inhibits alpha1-PI release from Caco-2 colonocytes treated with IL-1beta. It is therefore likely that anti-inflammatory actions of butyrate occur via a mechanism that does not involve direct regulation of cytokine-induced anti-inflammatory protein expression in intestinal epithelial cells. more...
- Published
- 2001
- Full Text
- View/download PDF
7. Nonsteroidal anti-inflammatory drugs stimulate spermidine/spermine acetyltransferase and deplete polyamine content in colon cancer cells
- Author
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Jürgen Stein, N. Dauletbaev, Vladan Milovic, and Lyudmila Turchanowa
- Subjects
Cell growth ,Colorectal cancer ,Clinical Biochemistry ,General Medicine ,Pharmacology ,Biology ,medicine.disease ,Biochemistry ,digestive system diseases ,Spermidine ,chemistry.chemical_compound ,chemistry ,Cell culture ,medicine ,Neoplastic cell ,Polyamine acetylation ,Polyamine ,Intracellular - Abstract
Background Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit colonic tumour-igenesis and have an established usefulness in cancer prevention. Because polyamines are essential for neoplastic cell growth, the aim of this study was to evaluate the effect of NSAIDs (indomethacin, a nonselective COX-1 and COX-2 inhibitor) on polyamine metabolism in colon cancer cells. Methods Both cell counting and thymidine incorporation into cellular DNA were used to assess colon cancer cell growth. Activities of polyamine-metabolising enzymes, polyamine content (HPLC) and ODC and c-myc protein expression (Western blot) were measured in colon cancer cells treated with indomethacin during logarithmic phase of proliferation. Results Indomethacin impaired growth of human colon cancer cells (Caco-2 and HCT-116). As a result, ornithine decarboxylase activity and c-myc protein expression were decreased. Treatment with indomethacin induced intracellular oxidant formation in colon cancer cells significantly increased the spermidine/spermine-acetyltrasferase activity (SSAT) and enhanced polyamine acetylation and efflux from colon cancer cells. Impairment of cell growth by indomethacin could not be reversed by exogenous polyamines. Conclusion Taken together, our results suggest that NSAIDs affect polyamine metabolism in colon cancer cells by inducing SSAT activity, and that polyamine depletion in NSAID-treated colon cancer cells is mainly due to enhanced polyamine acetylation and irreversible depletion of intracellular polyamine pools. more...
- Published
- 2001
- Full Text
- View/download PDF
8. Influence of physical exercise on polyamine synthesis in the rat skeletal muscle
- Author
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Vladan Milovic, Wolfgang F. Caspary, Jürgen Stein, V A Rogozkin, B I Feldkoren, and Lyudmila Turchanowa
- Subjects
Soleus muscle ,medicine.medical_specialty ,Muscle adaptation ,Clinical Biochemistry ,Spermine ,Skeletal muscle ,General Medicine ,Biology ,Biochemistry ,Ornithine decarboxylase ,Spermidine ,chemistry.chemical_compound ,Endocrinology ,medicine.anatomical_structure ,chemistry ,Internal medicine ,medicine ,Putrescine ,Polyamine - Abstract
Background Physical exercise and testosterone administration result in a series of adaptive anabolic phenomena in the skeletal muscle. The role of polyamines in these processes has been poorly explored. Design We measured the activities of polyamine-synthesising enzymes, ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (SAMDC) and polyamine content in skeletal muscle of male rats exposed to endurance or resistance exercise, or a single testosterone treatment. Soleus muscle (consisting mainly of slow-twitching oxidative fibres—STO) and extensor digitorum longus (mainly fast-twitching glycolytic muscle fibres—FTG) were analysed for polyamine content by HPLC, and ODC and SAMDC activity. Results Both endurance and resistance exercise induced a threefold increase in endogenous testosterone production. Two hours after exercise, ODC was increased in STO fibres, returning to baseline after 24 h; in FTG fibres the increase was less prominent. An increase in SAMDC activity occurred in a more sustained manner, with its peak 8 h after exercise. Polyamines were subsequently accumulated in both skeletal muscle fibres, with a rise in putrescine concentration after 2 h, and a fall corresponding to conversion of putrescine to spermidine and spermine by SAMDC. Single dose of 17α-methyltestosterone resulted in a similar increase in polyamine-synthesising enzyme activities and polyamine concentrations in the skeletal muscle. Conclusion Polyamine accumulation in the skeletal muscle after physical exercise is likely to occur secondary to testosterone production. Polyamines are apparently involved in the oxidative, but not in glycolytic processes related to muscle adaptation to exercise. more...
- Published
- 2000
- Full Text
- View/download PDF
9. Butyrate and the cytokine-induced alpha1-proteinase inhibitor release in intestinal epithelial cells
- Author
-
D, Faust, S, Hormann, M, Friedrich-Sander, V, Milovic, and J, Stein
- Subjects
Butyrates ,Interleukin-6 ,Tumor Necrosis Factor-alpha ,alpha 1-Antitrypsin ,Interleukin-8 ,Cytokines ,Humans ,Caco-2 Cells ,Intestinal Mucosa ,Inflammatory Bowel Diseases ,Interleukin-1 - Abstract
Alpha1-proteinase inhibitor (alpha1-PI), an anti-inflammatory protein thought to play a role in the intestinal inflammation, is synthesised by and released from the intestinal epithelial cells. IL-1beta is a key proinflammatory cytokine in the abnormal immune response that occurs in inflammatory bowel disease. Butyrate is a normal luminal constituent in the colon, known to be of benefit in preventing inflammatory bowel disease. Direct modes of action of butyrate in intestinal inflammation have been poorly studied so far. The aim of this study was to investigate the effects of butyrate on cytokine-mediated alpha1-PI release in intestinal epithelial cells.Differentiated Caco-2 cells were incubated with IL-1beta in the presence or absence of 2 mM butyrate. Alpha1-PI expression in the cells was evaluated by Western blot analysis and alpha1-PI release by ELISA.Treatment with butyrate alone had no effect on alpha1-PI expression in differentiated Caco-2 cells. However, treatment of the cells with 2 mM butyrate significantly reduced the alpha1-PI level in IL-1beta-treated cells. In the cell culture medium, the presence of butyrate impaired the IL-1beta-induced alpha1-PI release to 17-35%. The treatment induced no change in the number of detached cells or the percentage of viable cells.Our data show that butyrate inhibits alpha1-PI release from Caco-2 colonocytes treated with IL-1beta. It is therefore likely that anti-inflammatory actions of butyrate occur via a mechanism that does not involve direct regulation of cytokine-induced anti-inflammatory protein expression in intestinal epithelial cells. more...
- Published
- 2002
10. Effects of deoxycholate on human colon cancer cells: apoptosis or proliferation
- Author
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V, Milovic, I C, Teller, D, Faust, W F, Caspary, and J, Stein
- Subjects
Bile Acids and Salts ,Colonic Neoplasms ,Detergents ,Humans ,Apoptosis ,Caco-2 Cells ,Intestinal Mucosa ,HT29 Cells ,Cell Division ,Protein Kinase C ,Deoxycholic Acid - Abstract
Deoxycholic acid has long been attributed as a tumour promoter in the colon. It exerts its growth-related actions in a phorbol ester-like manner, by stimulating protein kinase C. The aim of this study was to investigate the effect of deoxycholic acid on proliferation and apoptosis in the colon, by exposing colon cancer cells to it in increasing concentrations.Human colon cancer cells (Caco-2 and HT-29) were treated with deoxycholate or its two structural isomers, 3-beta-12-alpha-dihydroxy-5-beta-cholan-24-oic acid and 3-alpha-12-beta-dihydroxy-5-beta-cholan-24-oic acid. Proliferation was evaluated by cell counting, and apoptosis by estimating percentage cell survival and assessment of nuclear morphology.Within the concentration range of up to 20 microM, deoxycholate stimulated growth of both human colon cancer cell lines. Its growth-promoting effect was abolished after inhibition of protein kinase C. At concentrations above 100 microM, deoxycholate induced apoptosis in both cell lines. Epimers of deoxycholate were significantly less potent in stimulating growth.Low-dose deoxycholate stimulates colon cancer cell proliferation while100 micromol L(-1) of this secondary bile acid induces apoptosis in colon cancer cells. Deoxycholate might promote the likelihood of malignant transformation by increasing epithelial cell turnover in the colon. more...
- Published
- 2002
11. Nonsteroidal anti-inflammatory drugs stimulate spermidine/spermine acetyltransferase and deplete polyamine content in colon cancer cells
- Author
-
L, Turchanowa, N, Dauletbaev, V, Milovic, and J, Stein
- Subjects
Cyclooxygenase 2 Inhibitors ,Anti-Inflammatory Agents, Non-Steroidal ,Indomethacin ,Membrane Proteins ,Acetylation ,Ornithine Decarboxylase ,Oxidants ,Isoenzymes ,Proto-Oncogene Proteins c-myc ,Acetyltransferases ,Cyclooxygenase 2 ,Prostaglandin-Endoperoxide Synthases ,Colonic Neoplasms ,Polyamines ,Tumor Cells, Cultured ,Humans ,Cyclooxygenase Inhibitors ,Caco-2 Cells ,Cell Division - Abstract
Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit colonic tumourigenesis and have an established usefulness in cancer prevention. Because polyamines are essential for neoplastic cell growth, the aim of this study was to evaluate the effect of NSAIDs (indomethacin, a nonselective COX-1 and COX-2 inhibitor) on polyamine metabolism in colon cancer cells.Both cell counting and thymidine incorporation into cellular DNA were used to assess colon cancer cell growth. Activities of polyamine-metabolising enzymes, polyamine content (HPLC) and ODC and c-myc protein expression (Western blot) were measured in colon cancer cells treated with indomethacin during logarithmic phase of proliferation.Indomethacin impaired growth of human colon cancer cells (Caco-2 and HCT-116). As a result, ornithine decarboxylase activity and c-myc protein expression were decreased. Treatment with indomethacin induced intracellular oxidant formation in colon cancer cells significantly increased the spermidine/spermine-acetyltrasferase activity (SSAT) and enhanced polyamine acetylation and efflux from colon cancer cells. Impairment of cell growth by indomethacin could not be reversed by exogenous polyamines.Taken together, our results suggest that NSAIDs affect polyamine metabolism in colon cancer cells by inducing SSAT activity, and that polyamine depletion in NSAID-treated colon cancer cells is mainly due to enhanced polyamine acetylation and irreversible depletion of intracellular polyamine pools. more...
- Published
- 2001
12. Influence of physical exercise on polyamine synthesis in the rat skeletal muscle
- Author
-
L, Turchanowa, V A, Rogozkin, V, Milovic, B I, Feldkoren, W F, Caspary, and J, Stein
- Subjects
Male ,Adenosylmethionine Decarboxylase ,Physical Conditioning, Animal ,Biogenic Polyamines ,Animals ,Testosterone ,Rats, Wistar ,Muscle, Skeletal ,Ornithine Decarboxylase ,Rats - Abstract
Physical exercise and testosterone administration result in a series of adaptive anabolic phenomena in the skeletal muscle. The role of polyamines in these processes has been poorly explored.We measured the activities of polyamine-synthesising enzymes, ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (SAMDC) and polyamine content in skeletal muscle of male rats exposed to endurance or resistance exercise, or a single testosterone treatment. Soleus muscle (consisting mainly of slow-twitching oxidative fibres-STO) and extensor digitorum longus (mainly fast-twitching glycolytic muscle fibres-FTG) were analysed for polyamine content by HPLC, and ODC and SAMDC activity.Both endurance and resistance exercise induced a threefold increase in endogenous testosterone production. Two hours after exercise, ODC was increased in STO fibres, returning to baseline after 24 h; in FTG fibres the increase was less prominent. An increase in SAMDC activity occurred in a more sustained manner, with its peak 8 h after exercise. Polyamines were subsequently accumulated in both skeletal muscle fibres, with a rise in putrescine concentration after 2 h, and a fall corresponding to conversion of putrescine to spermidine and spermine by SAMDC. Single dose of 17alpha-methyltestosterone resulted in a similar increase in polyamine-synthesising enzyme activities and polyamine concentrations in the skeletal muscle.Polyamine accumulation in the skeletal muscle after physical exercise is likely to occur secondary to testosterone production. Polyamines are apparently involved in the oxidative, but not in glycolytic processes related to muscle adaptation to exercise. more...
- Published
- 2000
13. Characterization of putrescine transport across the intestinal epithelium: study using isolated brush border and basolateral membrane vesicles of the enterocyte
- Author
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Jürgen Stein, Vladan Milovic, Albrecht Piiper, Stefan Zeuzem, Wolfgang F. Caspary, and Ralf Gerhard
- Subjects
Paraquat ,Mitoguazone ,Brush border ,Enterocyte ,Clinical Biochemistry ,Biology ,Biochemistry ,Epithelium ,chemistry.chemical_compound ,medicine ,Putrescine ,Animals ,Epithelial polarity ,Organelles ,Polyamine transport ,Microvilli ,Vesicle ,Cell Membrane ,Osmolar Concentration ,Sodium ,Biological Transport ,General Medicine ,Apical membrane ,Intestines ,medicine.anatomical_structure ,chemistry ,Putrescine transport ,Biophysics ,Rabbits - Abstract
Putrescine transport was investigated in isolated brush border and basolateral membrane vesicles prepared from the rabbit enterocyte. Brush border vesicles were oriented right-side-out and basolateral vesicles inside-out, forming a model representing uptake and extrusion across the intestinal epithelium. Putrescine transport across both membranes was initially rapid, and 66% of the equilibrium uptake was achieved within the first minute. According to osmoplots and measurements at 4 degrees C, 20% of total incorporation presented binding to the membrane. In order to estimate actual uptake into the vesicles, Km was calculated from the differences in putrescine incorporation at 37 degrees C and 4 degrees C, and was 12.7 mumol L-1 for brush border uptake and 38.2 mumol L-1 for basolateral extrusion. Putrescine uptake into brush border and basolateral membrane vesicles was not enhanced in the presence of an Na+ gradient. When Na+ was substituted with an uncharged solute, mannitol, putrescine incorporation was increased, indicating that putrescine uptake is not Na(+)-dependent and that cations might interfere with the carrier. Paraquat and methylglyoxalbis(guanylhydrazone), known to share the polyamine transport system, inhibited putrescine incorporation in both membrane vesicle preparations. Basolateral carrier showed significantly higher sensitivity to cations. We conclude that putrescine uptake across the apical membrane and extrusion across the basolateral membrane of the enterocyte are mediated by two different and independent carriers which differ in their electrical properties. more...
- Published
- 1995
14. Characterization of putrescine transport across the intestinal epithelium: study using isolated brush border and basolateral membrane vesicles of the enterocyte
- Author
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MILOVIC, V., primary, STEIN, J., additional, PIIPER, A., additional, GERHARD, R., additional, ZEUZEM, S., additional, and CASPARY, W. F., additional
- Published
- 1995
- Full Text
- View/download PDF
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