Fetal esophageal ligation induces expression of vascular endothelial growth factor messenger ribonucleic acid in fetal membranes

Larry C. Matsumoto, Ljubica Bogic, Robert A. Brace, Cecilia Cheung

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

OBJECTIVE: Obstruction of the fetal esophagus does not always produce the expected polyhydramnios. This is because of increased intramembranous absorption of amniotic fluid into the fetal circulation. A possible mediator for this increased absorption is vascular endothelial growth factor (VEGF). The present objective was to explore whether VEGF gene expression and action would be induced in fetal membranes and placentas of ovine fetuses after esophageal ligation. STUDY DESIGN: Five late-gestation fetal sheep underwent esophageal ligation and 5 served as control animals. On postoperative day 9, amnion, chorion, and placenta were collected for cellular localization and quantitation of VEGF messenger ribonucleic acid by in situ hybridization and Northern blot analysis. Reverse-transcription polymerase chain reaction was used to identify the VEGF molecular forms. Immunostaining with Ki-67 antibody was used to determine the proliferation of vascular endothelium in the fetal membranes and placentas. RESULTS: VEGF messenger ribonucleic acid was localized in amniotic epithelium, chorionic cytotrophoblast, and cytotrophoblast of the placenta. VEGF164 was the major transcript expressed in these tissues. The abundance of VEGF messenger ribonucleic acid in the amnion and chorion, but not in the placenta, was significantly increased in the ligated fetuses in comparison with the control fetuses. The proliferation of the intramembranous blood vessel endothelium was greater in the ligated fetuses than in the control fetuses. CONCLUSION: The levels of VEGF messenger ribonucleic acid and the proliferation of vascular endothelium in the amnion and chorion increased after fetal esophageal ligation. This provides a possible mechanism for the enhanced intramembranous absorption of amniotic fluid through increased vascularity and permeability of the fetal membranes, thus ameliorating the development of polyhydramnios. We speculate that the signal(s) that mediate the increase in VEGF expression is present in either the fetal urine or the fetal lung secretions, or both.

Original languageEnglish (US)
Pages (from-to)175-184
Number of pages10
JournalAmerican Journal of Obstetrics and Gynecology
Volume184
Issue number2
DOIs
StatePublished - 2001
Externally publishedYes

Fingerprint

Extraembryonic Membranes
Vascular Endothelial Growth Factor A
Ligation
RNA
Placenta
Fetus
Chorion
Amnion
Polyhydramnios
Vascular Endothelium
Trophoblasts
Amniotic Fluid
Sheep
Northern Blotting
Esophagus
Reverse Transcription
Endothelium
In Situ Hybridization
Blood Vessels
Permeability

Keywords

  • Amnion
  • Chorion
  • Esophagus
  • Fetus
  • Polyhydramnios
  • Vascular endothelial growth factor
  • VEGF

ASJC Scopus subject areas

  • Medicine(all)
  • Obstetrics and Gynecology

Cite this

Fetal esophageal ligation induces expression of vascular endothelial growth factor messenger ribonucleic acid in fetal membranes. / Matsumoto, Larry C.; Bogic, Ljubica; Brace, Robert A.; Cheung, Cecilia.

In: American Journal of Obstetrics and Gynecology, Vol. 184, No. 2, 2001, p. 175-184.

Research output: Contribution to journalArticle

Matsumoto, Larry C. ; Bogic, Ljubica ; Brace, Robert A. ; Cheung, Cecilia. / Fetal esophageal ligation induces expression of vascular endothelial growth factor messenger ribonucleic acid in fetal membranes. In: American Journal of Obstetrics and Gynecology. 2001 ; Vol. 184, No. 2. pp. 175-184.
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abstract = "OBJECTIVE: Obstruction of the fetal esophagus does not always produce the expected polyhydramnios. This is because of increased intramembranous absorption of amniotic fluid into the fetal circulation. A possible mediator for this increased absorption is vascular endothelial growth factor (VEGF). The present objective was to explore whether VEGF gene expression and action would be induced in fetal membranes and placentas of ovine fetuses after esophageal ligation. STUDY DESIGN: Five late-gestation fetal sheep underwent esophageal ligation and 5 served as control animals. On postoperative day 9, amnion, chorion, and placenta were collected for cellular localization and quantitation of VEGF messenger ribonucleic acid by in situ hybridization and Northern blot analysis. Reverse-transcription polymerase chain reaction was used to identify the VEGF molecular forms. Immunostaining with Ki-67 antibody was used to determine the proliferation of vascular endothelium in the fetal membranes and placentas. RESULTS: VEGF messenger ribonucleic acid was localized in amniotic epithelium, chorionic cytotrophoblast, and cytotrophoblast of the placenta. VEGF164 was the major transcript expressed in these tissues. The abundance of VEGF messenger ribonucleic acid in the amnion and chorion, but not in the placenta, was significantly increased in the ligated fetuses in comparison with the control fetuses. The proliferation of the intramembranous blood vessel endothelium was greater in the ligated fetuses than in the control fetuses. CONCLUSION: The levels of VEGF messenger ribonucleic acid and the proliferation of vascular endothelium in the amnion and chorion increased after fetal esophageal ligation. This provides a possible mechanism for the enhanced intramembranous absorption of amniotic fluid through increased vascularity and permeability of the fetal membranes, thus ameliorating the development of polyhydramnios. We speculate that the signal(s) that mediate the increase in VEGF expression is present in either the fetal urine or the fetal lung secretions, or both.",
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N2 - OBJECTIVE: Obstruction of the fetal esophagus does not always produce the expected polyhydramnios. This is because of increased intramembranous absorption of amniotic fluid into the fetal circulation. A possible mediator for this increased absorption is vascular endothelial growth factor (VEGF). The present objective was to explore whether VEGF gene expression and action would be induced in fetal membranes and placentas of ovine fetuses after esophageal ligation. STUDY DESIGN: Five late-gestation fetal sheep underwent esophageal ligation and 5 served as control animals. On postoperative day 9, amnion, chorion, and placenta were collected for cellular localization and quantitation of VEGF messenger ribonucleic acid by in situ hybridization and Northern blot analysis. Reverse-transcription polymerase chain reaction was used to identify the VEGF molecular forms. Immunostaining with Ki-67 antibody was used to determine the proliferation of vascular endothelium in the fetal membranes and placentas. RESULTS: VEGF messenger ribonucleic acid was localized in amniotic epithelium, chorionic cytotrophoblast, and cytotrophoblast of the placenta. VEGF164 was the major transcript expressed in these tissues. The abundance of VEGF messenger ribonucleic acid in the amnion and chorion, but not in the placenta, was significantly increased in the ligated fetuses in comparison with the control fetuses. The proliferation of the intramembranous blood vessel endothelium was greater in the ligated fetuses than in the control fetuses. CONCLUSION: The levels of VEGF messenger ribonucleic acid and the proliferation of vascular endothelium in the amnion and chorion increased after fetal esophageal ligation. This provides a possible mechanism for the enhanced intramembranous absorption of amniotic fluid through increased vascularity and permeability of the fetal membranes, thus ameliorating the development of polyhydramnios. We speculate that the signal(s) that mediate the increase in VEGF expression is present in either the fetal urine or the fetal lung secretions, or both.

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