Arachidonic acid incorporation into lipids of term human amnion

Olson, David M.; Smieja, Zofia

doi:10.1016/s0002-9378(88)80187-x

Cited by 16 publications

(4 citation statements)

References 17 publications

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“…The proportion of arachidonic acid in phosphatidylethanolamine is also lower than that previously reported in freshly dispersed amnion cells following labeling with radioactive arachi¬ donate acid (25). The difference between the distribution found in the present study and that reported by others (25) might be explained if arachidonic acid was preferentially released from phosphatidylethanolamine during this 24-h period. The difference between the distribution found in the present study and that reported by others (25) might be explained if arachidonic acid was preferentially released from phosphatidylethanolamine during this 24-h period.…”

Section: Discussioncontrasting

confidence: 79%

“…This is unlikely to be due to hydrolysis of plasmalogen because the methods used specifically guarded against this and by using confluent amnion cells we found concentrations of phosphatidylethanolamine (unpublished) that were com¬ parable with published data (24). The proportion of arachidonic acid in phosphatidylethanolamine is also lower than that previously reported in freshly dispersed amnion cells following labeling with radioactive arachi¬ donate acid (25). However, it should be remembered that in the present study the cells have been incubated for a further 24 h in the absence of radioactivity and the distribution of radioactivity in the lipids represents that remaining after this period.…”

Section: Discussionsupporting

confidence: 61%

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Studies on the action of dexamethasone on prostaglandin production by freshly dispersed amnion cells

Gibb

Breton²

1993

Acta Endocrinologica

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The human amnion may be an important source of prostaglandins (PGs) during pregnancy and possibly labor. Glucocorticoids stimulate PG production in confluent amnion cell cultures, but in freshly dispersed cells they inhibit PG production. The purpose of the present study was to determine if this inhibitory effect occurred at the level of arachidonic acid release from lipids. Cells were labeled with radioactive arachidonate and the release of radioactivity was measured in the presence or absence of dexamethasone. No significant effect of dexamethasone treatment was observed. The possibility that glucocorticoid treatment inhibited the release of arachidonate from a specific species of phospholipid was also examined. However, no difference was found in the distribution of arachidonate between lipids isolated from glucocorticoid-treated and untreated cells. Furthermore, dexamethasone treatment did not alter the lipocortin 1 and 2 content of dispersed cells, determined following sodium dodecyl sulfate polyacrylamide gel electrophoresis and immunoblotting. These studies indicate that the inhibition of prostaglandin production by dispersed amnion cells by glucocorticoids most likely occurs at a point distal to arachidonic acid release.

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Section: Discussioncontrasting

confidence: 79%

Section: Discussionsupporting

confidence: 61%

Studies on the action of dexamethasone on prostaglandin production by freshly dispersed amnion cells

Gibb

Breton²

1993

Acta Endocrinologica

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“…Olson and Smieja did not find any significant difference between the ability of dispersed amnion cells to incorporate radioactive arachidonate before and after labor. 89 Despite these discrepancies, the data agree in that there is no decrease in the rate of arachidonate reacylation in association with labor, suggesting that such a mechanism may not be responsible for the increased availability of arachidonate in the amnion at the time of parturition.…”

Section: Other Pathways Of Arachidonate Releasementioning

confidence: 84%

Intrauterine Tissue Prostaglandin Synthesis: Regulatory Mechanisms

Olson¹,

Zakár²

1993

Semin Reprod Med

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“…The lipid composition of the fetal membranes as well as the turnover of lipids and membrane phospholipids in the amnion are well characterized [10][11][12], In particular, lecithin has been demonstrated to be the major phospho lipid in the amnion, but it is not so abundant in the cho rion [10. 11].…”

Section: Introductionmentioning

confidence: 99%

Betamethasone-Induced Lecithin Release in vitro from the Fetal Membranes

Vesce

Pareschi²,

Travagli³

et al. 1992

Gynecol Obstet Invest

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Lecithin release from fetal membranes and placental tissue was assayed in basal conditions as well as under betamethasone administration. In the absence of the steroid, amnion and chorion released lecithin as a function of incubation time. Both tissues responded to betamethasone by increasing the lecithin release, the amnion exhibited a higher basal level and a greater responsiveness to the hormone than the chorion. Basal lecithin release from placental tissue was unaffected by any steroid concentration.

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Arachidonic acid incorporation into lipids of term human amnion

Cited by 16 publications

References 17 publications

Studies on the action of dexamethasone on prostaglandin production by freshly dispersed amnion cells

Studies on the action of dexamethasone on prostaglandin production by freshly dispersed amnion cells

Intrauterine Tissue Prostaglandin Synthesis: Regulatory Mechanisms

Betamethasone-Induced Lecithin Release in vitro from the Fetal Membranes

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