Paracrine interactions between platelet-activating factor and prostaglandins in hormonally-treated human luteal phase endometrium in vitro

A. A. Alecozay, M. J K Harper, Robert S Schenken, D. J. Hanahan

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Stromal cells and epithelial glands were separated after enzymic digestion of specimens obtained from 27 women at hysterectomy or endometrial biopsy during the luteal phase, and then cultured to confluence in vitro. PGF release into the culture medium (mean ± s.e.m.: ng/mg protein/24 h) from gland cell cultures was not changed by oestradiol (17.6 ± 1.3 for control and 25.5 ± 2.8 for respectively). However, in the presence of oestradiol, PAF (5 ng/ml) significantly elevated PGE release to 44.2 ± 5.8. No stimulation was observed in the presence of progesterone. Stromal cell medium had no effect on PGF release in gland cell cultures. PGE release was always much lower in stromal cell cultures than in glands (control: 4.7 ± 0.6). PAF stimulated PGE release in the presence of oestradiol in these cells also; gland cell medium was without effect. In co-cultures of glandular and stromal cells, PGE release was more similar to that seen in gland cell cultures, with PAF being stimulatory under the influence of oestradiol. PGF release into the medium from the same gland cell cultures was significantly elevated by hormonal treatment, being greatest (62.0 ± 11.3) with oestradiol alone, and was strongly inhibited in all wells by addition of PAF and stromal cell medium. In stromal cell cultures without hormonal addition, PGF levels (15.0 ± 2.4) were similar to those seen in glands (18.1 ± 3.1), and no stimulation was achieved by oestradiol (29.6 ± 5.9). PAF was inhibitory on PGF release, while gland cell medium was without effect. Co-cultures gave PGF values general1y similar to those of stromal cells; oestradiol was again stimulatory (55.0 ± 9.3). PAF was significantly inhibitory in the presence of oestradiol. PAF (mean ± s.e.m.: pmol/mg protein/24 h using a platelet serotonin release assay) in stromal cells was significantly increased from control [M199 alone] (0.31 ± 0.12) by progesterone (1.00 ± 0.17). Addition of PGE-2 (7.5 ng/ml) to progesterone-treated wells further increased-PAF concentration (5.34 ± 0.09), but was without effect in wells receiving oestradiol alone. Wells exposed to both hormones exhibited an intermediate response. Similar results were obtained with addition of gland cell culture medium, presumably due to its endogenous PGE content. In co-cultures, PAF concentrations were significantly elevated by progesterone alone (4.78 ± 0.78) or when combined with oestradiol (2.38 ± 0.51), but not by oestradiol alone. Treatment with PGE-2 caused no additional stimulation. In summary, PAF in stromal cells was increased by PGE-2 in the presence of progesterone, while PGE from gland cells was increased and PGF decreased by PAF in the presence of oestradiol. Gland cell medium exerted effects consistent with the presence of endogenous PGE-2. These results suggest a paracrine interaction between PAF and PGs in regulation of endometrial cell function.

Original languageEnglish (US)
Pages (from-to)301-312
Number of pages12
JournalJournal of Reproduction and Fertility
Volume91
Issue number1
StatePublished - 1991

Fingerprint

Luteal Phase
Platelet Activating Factor
Endometrium
Prostaglandins
Estradiol
Prostaglandins E
Stromal Cells
Prostaglandins F
Cell Culture Techniques
Progesterone
Coculture Techniques
Culture Media
In Vitro Techniques
Hysterectomy
Digestion
Serotonin
Proteins
Blood Platelets
Hormones

Keywords

  • endometrium
  • human
  • PAF
  • platelet-activating factor
  • prostaglandins

ASJC Scopus subject areas

  • Obstetrics and Gynecology
  • Embryology
  • Developmental Biology
  • Molecular Biology
  • Physiology

Cite this

Paracrine interactions between platelet-activating factor and prostaglandins in hormonally-treated human luteal phase endometrium in vitro. / Alecozay, A. A.; Harper, M. J K; Schenken, Robert S; Hanahan, D. J.

In: Journal of Reproduction and Fertility, Vol. 91, No. 1, 1991, p. 301-312.

Research output: Contribution to journalArticle

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T1 - Paracrine interactions between platelet-activating factor and prostaglandins in hormonally-treated human luteal phase endometrium in vitro

AU - Alecozay, A. A.

AU - Harper, M. J K

AU - Schenken, Robert S

AU - Hanahan, D. J.

PY - 1991

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N2 - Stromal cells and epithelial glands were separated after enzymic digestion of specimens obtained from 27 women at hysterectomy or endometrial biopsy during the luteal phase, and then cultured to confluence in vitro. PGF release into the culture medium (mean ± s.e.m.: ng/mg protein/24 h) from gland cell cultures was not changed by oestradiol (17.6 ± 1.3 for control and 25.5 ± 2.8 for respectively). However, in the presence of oestradiol, PAF (5 ng/ml) significantly elevated PGE release to 44.2 ± 5.8. No stimulation was observed in the presence of progesterone. Stromal cell medium had no effect on PGF release in gland cell cultures. PGE release was always much lower in stromal cell cultures than in glands (control: 4.7 ± 0.6). PAF stimulated PGE release in the presence of oestradiol in these cells also; gland cell medium was without effect. In co-cultures of glandular and stromal cells, PGE release was more similar to that seen in gland cell cultures, with PAF being stimulatory under the influence of oestradiol. PGF release into the medium from the same gland cell cultures was significantly elevated by hormonal treatment, being greatest (62.0 ± 11.3) with oestradiol alone, and was strongly inhibited in all wells by addition of PAF and stromal cell medium. In stromal cell cultures without hormonal addition, PGF levels (15.0 ± 2.4) were similar to those seen in glands (18.1 ± 3.1), and no stimulation was achieved by oestradiol (29.6 ± 5.9). PAF was inhibitory on PGF release, while gland cell medium was without effect. Co-cultures gave PGF values general1y similar to those of stromal cells; oestradiol was again stimulatory (55.0 ± 9.3). PAF was significantly inhibitory in the presence of oestradiol. PAF (mean ± s.e.m.: pmol/mg protein/24 h using a platelet serotonin release assay) in stromal cells was significantly increased from control [M199 alone] (0.31 ± 0.12) by progesterone (1.00 ± 0.17). Addition of PGE-2 (7.5 ng/ml) to progesterone-treated wells further increased-PAF concentration (5.34 ± 0.09), but was without effect in wells receiving oestradiol alone. Wells exposed to both hormones exhibited an intermediate response. Similar results were obtained with addition of gland cell culture medium, presumably due to its endogenous PGE content. In co-cultures, PAF concentrations were significantly elevated by progesterone alone (4.78 ± 0.78) or when combined with oestradiol (2.38 ± 0.51), but not by oestradiol alone. Treatment with PGE-2 caused no additional stimulation. In summary, PAF in stromal cells was increased by PGE-2 in the presence of progesterone, while PGE from gland cells was increased and PGF decreased by PAF in the presence of oestradiol. Gland cell medium exerted effects consistent with the presence of endogenous PGE-2. These results suggest a paracrine interaction between PAF and PGs in regulation of endometrial cell function.

AB - Stromal cells and epithelial glands were separated after enzymic digestion of specimens obtained from 27 women at hysterectomy or endometrial biopsy during the luteal phase, and then cultured to confluence in vitro. PGF release into the culture medium (mean ± s.e.m.: ng/mg protein/24 h) from gland cell cultures was not changed by oestradiol (17.6 ± 1.3 for control and 25.5 ± 2.8 for respectively). However, in the presence of oestradiol, PAF (5 ng/ml) significantly elevated PGE release to 44.2 ± 5.8. No stimulation was observed in the presence of progesterone. Stromal cell medium had no effect on PGF release in gland cell cultures. PGE release was always much lower in stromal cell cultures than in glands (control: 4.7 ± 0.6). PAF stimulated PGE release in the presence of oestradiol in these cells also; gland cell medium was without effect. In co-cultures of glandular and stromal cells, PGE release was more similar to that seen in gland cell cultures, with PAF being stimulatory under the influence of oestradiol. PGF release into the medium from the same gland cell cultures was significantly elevated by hormonal treatment, being greatest (62.0 ± 11.3) with oestradiol alone, and was strongly inhibited in all wells by addition of PAF and stromal cell medium. In stromal cell cultures without hormonal addition, PGF levels (15.0 ± 2.4) were similar to those seen in glands (18.1 ± 3.1), and no stimulation was achieved by oestradiol (29.6 ± 5.9). PAF was inhibitory on PGF release, while gland cell medium was without effect. Co-cultures gave PGF values general1y similar to those of stromal cells; oestradiol was again stimulatory (55.0 ± 9.3). PAF was significantly inhibitory in the presence of oestradiol. PAF (mean ± s.e.m.: pmol/mg protein/24 h using a platelet serotonin release assay) in stromal cells was significantly increased from control [M199 alone] (0.31 ± 0.12) by progesterone (1.00 ± 0.17). Addition of PGE-2 (7.5 ng/ml) to progesterone-treated wells further increased-PAF concentration (5.34 ± 0.09), but was without effect in wells receiving oestradiol alone. Wells exposed to both hormones exhibited an intermediate response. Similar results were obtained with addition of gland cell culture medium, presumably due to its endogenous PGE content. In co-cultures, PAF concentrations were significantly elevated by progesterone alone (4.78 ± 0.78) or when combined with oestradiol (2.38 ± 0.51), but not by oestradiol alone. Treatment with PGE-2 caused no additional stimulation. In summary, PAF in stromal cells was increased by PGE-2 in the presence of progesterone, while PGE from gland cells was increased and PGF decreased by PAF in the presence of oestradiol. Gland cell medium exerted effects consistent with the presence of endogenous PGE-2. These results suggest a paracrine interaction between PAF and PGs in regulation of endometrial cell function.

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