Induction of VE-cadherin in rat placental trophoblasts by VEGF through a NO-dependent pathway

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Vascular endothelial-cadherin (VE-cadherin), a calcium-dependent homotypic adhesion molecule, contributes to endothelial assembly and VEGF-mediated survival during angiogenesis. In human term placentas, villous vessels and extravillous cytotrophoblasts express VE-cadherin. Therefore, the purpose of this study was to examine if VEGF modulated placental development by increasing the expression of VE-cadherin in rat placentas. Placental tissues from rats on gestation days 14 (G14), 18 (G18) and 21 (G21) were used. Western blot analysis and immunohistochemistry were performed to detect the protein abundance and the distribution of VE-cadherin. A nitric oxide analyzer was used to measure the released nitric oxide (NO) from placental explant culture. With the progression of pregnancy, the abundance of VE-cadherin and the intensity of the immunoreactive staining for VE-cadherin in endovascular trophoblasts and labyrinth trophoblasts were decreased. In explant culture, VEGF (0.01-1.0 ng/ml) increased the protein abundance of VE-cadherin. SNP (an NO donor) or l-arginine (substrate for eNOS) induced the expression of VE-cadherin with the increase of NO production. l-NAME (a NOS inhibitor) reduced the VEGF-increased expression and l-arginine reversed the inhibitory effect of l-NAME. In conclusion, VEGF plays an important role in placental development by the induction of VE-cadherin in trophoblasts, which, in part, maintains the survival of labyrinth trophoblast in rat placentas.

Original languageEnglish
Pages (from-to)234-241
Number of pages8
JournalPlacenta
Volume26
Issue number2-3
DOIs
Publication statusPublished - 2005 Feb 1

Fingerprint

Trophoblasts
Vascular Endothelial Growth Factor A
Nitric Oxide
Placenta
Placentation
Inner Ear
Arginine
cadherin 5
Pregnancy
Nitric Oxide Donors
Single Nucleotide Polymorphism
Proteins
Western Blotting
Immunohistochemistry
Staining and Labeling
Calcium
Survival

All Science Journal Classification (ASJC) codes

  • Obstetrics and Gynaecology

Cite this

@article{8480f56416854198be4b83cd2d5242a4,
title = "Induction of VE-cadherin in rat placental trophoblasts by VEGF through a NO-dependent pathway",
abstract = "Vascular endothelial-cadherin (VE-cadherin), a calcium-dependent homotypic adhesion molecule, contributes to endothelial assembly and VEGF-mediated survival during angiogenesis. In human term placentas, villous vessels and extravillous cytotrophoblasts express VE-cadherin. Therefore, the purpose of this study was to examine if VEGF modulated placental development by increasing the expression of VE-cadherin in rat placentas. Placental tissues from rats on gestation days 14 (G14), 18 (G18) and 21 (G21) were used. Western blot analysis and immunohistochemistry were performed to detect the protein abundance and the distribution of VE-cadherin. A nitric oxide analyzer was used to measure the released nitric oxide (NO) from placental explant culture. With the progression of pregnancy, the abundance of VE-cadherin and the intensity of the immunoreactive staining for VE-cadherin in endovascular trophoblasts and labyrinth trophoblasts were decreased. In explant culture, VEGF (0.01-1.0 ng/ml) increased the protein abundance of VE-cadherin. SNP (an NO donor) or l-arginine (substrate for eNOS) induced the expression of VE-cadherin with the increase of NO production. l-NAME (a NOS inhibitor) reduced the VEGF-increased expression and l-arginine reversed the inhibitory effect of l-NAME. In conclusion, VEGF plays an important role in placental development by the induction of VE-cadherin in trophoblasts, which, in part, maintains the survival of labyrinth trophoblast in rat placentas.",
author = "Chih-Ching Chang and Chang, {Torng Yuo} and Chen-Hsiang Yu and Mei-Ling Tsai",
year = "2005",
month = "2",
day = "1",
doi = "10.1016/j.placenta.2004.06.002",
language = "English",
volume = "26",
pages = "234--241",
journal = "Placenta",
issn = "0143-4004",
publisher = "W.B. Saunders Ltd",
number = "2-3",

}

Induction of VE-cadherin in rat placental trophoblasts by VEGF through a NO-dependent pathway. / Chang, Chih-Ching; Chang, Torng Yuo; Yu, Chen-Hsiang; Tsai, Mei-Ling.

In: Placenta, Vol. 26, No. 2-3, 01.02.2005, p. 234-241.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Induction of VE-cadherin in rat placental trophoblasts by VEGF through a NO-dependent pathway

AU - Chang, Chih-Ching

AU - Chang, Torng Yuo

AU - Yu, Chen-Hsiang

AU - Tsai, Mei-Ling

PY - 2005/2/1

Y1 - 2005/2/1

N2 - Vascular endothelial-cadherin (VE-cadherin), a calcium-dependent homotypic adhesion molecule, contributes to endothelial assembly and VEGF-mediated survival during angiogenesis. In human term placentas, villous vessels and extravillous cytotrophoblasts express VE-cadherin. Therefore, the purpose of this study was to examine if VEGF modulated placental development by increasing the expression of VE-cadherin in rat placentas. Placental tissues from rats on gestation days 14 (G14), 18 (G18) and 21 (G21) were used. Western blot analysis and immunohistochemistry were performed to detect the protein abundance and the distribution of VE-cadherin. A nitric oxide analyzer was used to measure the released nitric oxide (NO) from placental explant culture. With the progression of pregnancy, the abundance of VE-cadherin and the intensity of the immunoreactive staining for VE-cadherin in endovascular trophoblasts and labyrinth trophoblasts were decreased. In explant culture, VEGF (0.01-1.0 ng/ml) increased the protein abundance of VE-cadherin. SNP (an NO donor) or l-arginine (substrate for eNOS) induced the expression of VE-cadherin with the increase of NO production. l-NAME (a NOS inhibitor) reduced the VEGF-increased expression and l-arginine reversed the inhibitory effect of l-NAME. In conclusion, VEGF plays an important role in placental development by the induction of VE-cadherin in trophoblasts, which, in part, maintains the survival of labyrinth trophoblast in rat placentas.

AB - Vascular endothelial-cadherin (VE-cadherin), a calcium-dependent homotypic adhesion molecule, contributes to endothelial assembly and VEGF-mediated survival during angiogenesis. In human term placentas, villous vessels and extravillous cytotrophoblasts express VE-cadherin. Therefore, the purpose of this study was to examine if VEGF modulated placental development by increasing the expression of VE-cadherin in rat placentas. Placental tissues from rats on gestation days 14 (G14), 18 (G18) and 21 (G21) were used. Western blot analysis and immunohistochemistry were performed to detect the protein abundance and the distribution of VE-cadherin. A nitric oxide analyzer was used to measure the released nitric oxide (NO) from placental explant culture. With the progression of pregnancy, the abundance of VE-cadherin and the intensity of the immunoreactive staining for VE-cadherin in endovascular trophoblasts and labyrinth trophoblasts were decreased. In explant culture, VEGF (0.01-1.0 ng/ml) increased the protein abundance of VE-cadherin. SNP (an NO donor) or l-arginine (substrate for eNOS) induced the expression of VE-cadherin with the increase of NO production. l-NAME (a NOS inhibitor) reduced the VEGF-increased expression and l-arginine reversed the inhibitory effect of l-NAME. In conclusion, VEGF plays an important role in placental development by the induction of VE-cadherin in trophoblasts, which, in part, maintains the survival of labyrinth trophoblast in rat placentas.

UR - http://www.scopus.com/inward/record.url?scp=13844299068&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=13844299068&partnerID=8YFLogxK

U2 - 10.1016/j.placenta.2004.06.002

DO - 10.1016/j.placenta.2004.06.002

M3 - Article

VL - 26

SP - 234

EP - 241

JO - Placenta

JF - Placenta

SN - 0143-4004

IS - 2-3

ER -