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Biomedical subjects

S Murota

Publications and source records attributed to S Murota.

At least 217 records · Page 12Linked to original sources
PubMed1982

Comparative effect of lipoxygenase products of arachidonic acid on rat aortic smooth muscle cell migration.

We investigated the effects of mono-hydroxyeicosatetraenoic acids (HETEs) and N-formyl-methionyl-leucyl-phenylalanine (F-Met-Leu-Phe) on rat aortic smooth muscle cell migration in modified Boyden chambers. 12-HETE showed the most potent stimulatory effect on smooth muscle cell migration among the mono-HETEs tested. The optimal concentrations for cell migration were 3 X 10(-15) and 3 X 10(-13) g/ml for 12-HETE and 10(-8) g/ml for 15-HETE, 5-HETE and F-Met-Leu-Phe were inactive with these cells. As 12-HETE is biosynthesized from arachidonic acid by the 12-lipoxygenase pathway in platelets and macrophages, and 15-HETE by the 15-lipoxygenase pathway in granulocytes, the present results indicate an important role for such cells in the early phase of atherosclerosis.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1982

Platelets stimulate aortic smooth muscle cell migration in vitro. Involvement of 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid.

The migration of rat aortic smooth muscle cells was measured in modified Boyden chambers. Smooth muscle cells were motile in vitro and their migration was stimulated (time- and dose-dependently) by a platelet-derived factor. Treatment of platelets with indomethacin resulted in a significant increase in smooth muscle cell migration, whereas treatment with 5,8,10,14-eicosatetraenoic acid inhibited it. Purified 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid at a very low concentration (6 x 10(-15)-6 x 10(-13) g/ml) significantly stimulated smooth muscle cell migration. The locomotion induced by 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid was chemokinetic. These findings point to the physiological importance of a platelet 12-lipoxygenase product of arachidonic acid in the early phase of atherosclerosis.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1982

Comparison of prostaglandin biosynthetic activity between porcine aortic endothelial and smooth muscle cells in culture.

Prostaglandin biosynthetic activity of miniature-pig aortic endothelial cells was compared with that of smooth muscle cells in culture. When used as homogenates, endothelial cells produced mainly PGE2 and 6-ketoPGF1 alpha (degradated product of PGI2) from arachidonic acid, while they produced a large amount of PGF2 alpha in addition to these when used as intact cells. Intact smooth muscle cells and their homogenates produced PGE2 as a major product. 6-KetoPGF1 alpha was produced by smooth muscle cells in the first few generations and became undetectable after several cultivations. 6-KetoPGF1 alpha and PGE2 were produced by intact or endothelium-depleted aortas. Our results suggest that both endothelial cells and smooth muscle cells in porcine aorta possess PGI2 and PGE2 biosynthetic activities. The subcultivation of smooth muscle cells, but not endothelial cells, in vitro resulted in the rapid disappearance of PGI2 synthetase activity. The PGI2 biosynthetic activity of endothelial cells was several fold higher than that of smooth muscle cells. Porcine smooth muscle cells' low ability to produce PGI2 may offer a reason why atherosclerosis is easily developed in pigs.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Effects of estradiol on the metabolism of arachidonic acid by aortas and platelets in rats.

We have previously reported that estradiol treatment stimulates prostacyclin production by cultured rat aortic smooth muscle cells, through the stimulation of fatty acid cyclooxygenase and prostacyclin synthetase activities. In order to see whether estradiol stimulates the fatty acid cyclooxygenase activity in platelets, intact rats were treated with estradiol, and thromboxane biosynthesis in platelets and prostacyclin production by aortas were investigated. Estradiol significantly stimulates prostacyclin production by aortas. However, no significant effect on thromboxane biosynthesis in platelets is observed. Our present results support the idea that estradiol would be a protective hormone in atherosclerotic heart disease.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1981

Effect of sodium n-butyrate on induction of prostaglandin synthase activity in cloned mastocytoma P-815 2-E-6 cells.

Treatment of a cloned mastocytoma P-815 cell line (2-E-6) with 1 mM-sodium n-butyrate for 40h induced prostaglandin synthase activity and arrested cell growth. The induction of enzyme activity by n-butyrate was not associated with suppression of DNA synthesis, since hydroxyurea had no effect on prostaglandin synthase induction. The effect of sodium n-butyrate was reversible. Experiments with cycloheximide and actinomycin D showed that the induction of prostaglandin synthase activity involved synthesis de novo of protein and RNA. The time of half-maximal induction of the newly synthesized RNA for prostaglandin synthase activity was estimated as about 15h, which is similar to the generation time of the cells. Selective induction of fatty acid cyclo-oxygenase activity by sodium n-butyrate was suggested by the following two pieces of experimental evidence. (1) There was no significant difference between treated and untreated cells in the activities of radioactive prostaglandin H2 conversion into individual prostaglandins. (2) The incorporation of [3H]acetylsalicylic acid into the fraction equivalent to protein of mol.wt. approx. 75000 of sodium n-butyrate-treated cells was higher than that of untreated cells, on analysis of cell particulate fraction by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis. A high concentration (5 mM) of sodium propionate also induced prostaglandin synthesis, but other short-chain fatty acids, such as isobutyrate and sodium acetate, had no effect.

Animals↗
PubMed1981

Triiodothyronine stimulates prostacyclin production by rat aortic smooth muscle cells in culture.

The effect of triiodothyronine (T3) on prostacyclin production in rat aortic smooth muscle cells was investigated by using an intact cell assay system. T3 at its physiological concentrations has no significant effect on smooth muscle cell proliferation, but it does significantly stimulate prostacyclin production by the cells. Maximum stimulation of prostacyclin production is obtained when cells are treated with T3 for 4 consecutive days. The dose--response curve shows a linear relationship between the stimulation of prostacyclin production and T3 concentrations in the range 0.007--10 microgram/dl. The maximal prostacyclin production by T3-treated cells (at a concentration of 10 microgram/dl), is 270% compared with control cells. T3 treatment shows no significant effect on phospholipase (and/or lipase) activities. Our results suggest that thyroid hormone might play an important physiological role in the protection of arteries from atherosclerotic changes by stimulating prostacyclin production in arterial smooth muscle cells.

Animals↗
PubMed1981

Increased prostacyclin synthesizing activity in human ripening uterine cervix.

Homogenate of human uterine cervix at delivery were incubated with radioactive arachidonic acid. A major metabolite (conversion rate, approx. 20%) was identified with 6-ketoprostaglandin F1 alpha, a metabolite of prostacyclin. The 6-ketoprostaglandin F1 alpha production in the ripening cervix was more than 6 times per wet weight and 37 times per DNA as much as that in the non-pregnant cervix.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Effect of acute nitrogen dioxide exposure on the prostacyclin synthesis in lung.

The effect of acute nitrogen dioxide (NO2) exposure on prostacyclin synthesis in the rat lung was studied. Male Wistar rats were exposed to 5, 10, 15, 20 and 25 ppm NO2 for 24 h. Dose-dependent decrease in prostacyclin-synthesizing activities of both homogenized and intact lung was observed. This decrease in prostacyclin synthesis following NO2 exposure may be related to formation of lipid peroxides due to NO2 exposure and to damage of pulmonary epithelial cells and endothelial cells by NO2 exposure.

Air Pollutants↗
PubMed1980

Stimulation of prostacyclin biosynthetic activity by estradiol in rat aortic smooth muscle cells in culture.

Effects of estradio on cell proliferation and prostacyclin biosynthetic activity in cultured rat aortic smooth muscle cells are investigated. Prostacyclin is the major product formed from arachidonic acid by the cells, both in a cell-free homogenate system and in intact cells. When cells are treated with estradiol, no effect on cell proliferation is observed. However, a significantly stimulatory effect on prostacyclin biosynthetic activity in cells is evident. The maximal effect of estradiol on the stimulation of prostacyclin biosynthetic activity is observed after 5-day treatment of the cells with estradiol at its physiological concentration (10(-9) M). Our results support the idea that estradiol would be a protective hormone in atherosclerotic heart disease.

Adenosine Diphosphate↗
PubMed1980

Enhancement of prostaglandin synthesizing activity by the treatment with sodium n-butyrate on cloned mastocytoma cells and various other tissue cell lines.

We have compared the effects of n-butyrate on the prostaglandin synthesizing activities of cloned mouse mastocytoma cells, and various other tissue culture cell lines. Cells were treated with 1 mM n-butyrate for 40 hrs before harvesting. Prostaglandin synthesizing activities of the treated and the control cells were examined in a cell-free assay system. The treatment of some of the cloned mastocytoma cells with n-butyrate brought about the synthesis of prostaglandin D2, E2 and F2 alpha that were not synthesized by the control cells. The treatment of epithelial liver cells (BC-90) also resulted in the formation of 6-keto-prostaglandin F1 alpha which was not formed by the control cells. However, n-butyrate caused relatively small changes in the prostaglandin synthesizing activities of other clones of mastocytoma cells, mouse hepatoma cells, HeLa cells, rat granuloma cells and human embryonic fibroblasts. These data suggest differential effects of n-butyrate on different types of cultured cells.

Animals↗
PubMed1980

Effect of aging on the prostaglandin-synthesizing system in rat liver.

The effect of aging on the prostaglandin-synthesizing system in the rat liver was studied. No alteration in prostaglandin synthesis was observed during the period from 2 to 72 weeks, however, after 72 weeks the prostaglandin-synthesizing activity decreased gradually. At 92 weeks, the enzyme activity was down to 60% comparing with the young level. But the ratio of the production rate of prostaglandin E2 to that of prostaglandin F2 alpha remained constant throughout the experimental period. On the other hand, the activity of the liver in incorporating arachidonic acid into phospholipids increasing gradually with aging as a mirror image of prostaglandin synthesis. In young rats, the production of prostaglandins was significantly increased by phenobarbital-treatment, while in old rats this increase in prostaglandin synthesis failed to appear.

Aging↗