Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model.

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Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model. / Prados, M B; Solano, Maria Emilia; Friebe, A; Blois, S; Arck, Petra; Miranda, S.

in: J REPROD IMMUNOL, Jahrgang 89, Nr. 2, 2, 2011, S. 207-211.

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@article{67521b8a900149babbaec43e9fb7a670,
title = "Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model.",
abstract = "Sound stress exposure increases fetal loss via inflammatory pathways. Inflammation is known to up-regulate cell adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), which mediates the adhesion of leukocytes to the vascular endothelium. In this work, we studied the frequency of VCAM-1(+) vessels at the fetomaternal interface in stressed and non-stressed pregnant CBA/J female mice mated with DBA/2J (high fetal loss model) or BALB/c (low fetal loss model) males. The high fetal loss model had fewer large vessels on gestation day 6.5, and stress reduced the frequency of large vessels to a similar number in both high and low fetal loss models. In the high fetal loss model, however, the frequency of VCAM-1+ vessels was dramatically increased. This study shows that VCAM-1 expression is modulated by stress at the fetomaternal interface in abortion-prone cross-breeding.",
keywords = "Animals, Male, Female, Mice, Mice, Inbred BALB C, Pregnancy, *Gene Expression Regulation, *Stress, Physiological, Abortion, Spontaneous/*metabolism/pathology, Mice, Inbred CBA, Placenta/*metabolism/pathology, Vascular Cell Adhesion Molecule-1/*biosynthesis, Animals, Male, Female, Mice, Mice, Inbred BALB C, Pregnancy, *Gene Expression Regulation, *Stress, Physiological, Abortion, Spontaneous/*metabolism/pathology, Mice, Inbred CBA, Placenta/*metabolism/pathology, Vascular Cell Adhesion Molecule-1/*biosynthesis",
author = "Prados, {M B} and Solano, {Maria Emilia} and A Friebe and S Blois and Petra Arck and S Miranda",
year = "2011",
doi = "10.1016/j.jri.2011.01.021",
language = "English",
volume = "89",
pages = "207--211",
journal = "J REPROD IMMUNOL",
issn = "0165-0378",
publisher = "Elsevier Ireland Ltd",
number = "2",

}

RIS

TY - JOUR

T1 - Stress increases VCAM-1 expression at the fetomaternal interface in an abortion-prone mouse model.

AU - Prados, M B

AU - Solano, Maria Emilia

AU - Friebe, A

AU - Blois, S

AU - Arck, Petra

AU - Miranda, S

PY - 2011

Y1 - 2011

N2 - Sound stress exposure increases fetal loss via inflammatory pathways. Inflammation is known to up-regulate cell adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), which mediates the adhesion of leukocytes to the vascular endothelium. In this work, we studied the frequency of VCAM-1(+) vessels at the fetomaternal interface in stressed and non-stressed pregnant CBA/J female mice mated with DBA/2J (high fetal loss model) or BALB/c (low fetal loss model) males. The high fetal loss model had fewer large vessels on gestation day 6.5, and stress reduced the frequency of large vessels to a similar number in both high and low fetal loss models. In the high fetal loss model, however, the frequency of VCAM-1+ vessels was dramatically increased. This study shows that VCAM-1 expression is modulated by stress at the fetomaternal interface in abortion-prone cross-breeding.

AB - Sound stress exposure increases fetal loss via inflammatory pathways. Inflammation is known to up-regulate cell adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), which mediates the adhesion of leukocytes to the vascular endothelium. In this work, we studied the frequency of VCAM-1(+) vessels at the fetomaternal interface in stressed and non-stressed pregnant CBA/J female mice mated with DBA/2J (high fetal loss model) or BALB/c (low fetal loss model) males. The high fetal loss model had fewer large vessels on gestation day 6.5, and stress reduced the frequency of large vessels to a similar number in both high and low fetal loss models. In the high fetal loss model, however, the frequency of VCAM-1+ vessels was dramatically increased. This study shows that VCAM-1 expression is modulated by stress at the fetomaternal interface in abortion-prone cross-breeding.

KW - Animals

KW - Male

KW - Female

KW - Mice

KW - Mice, Inbred BALB C

KW - Pregnancy

KW - Gene Expression Regulation

KW - Stress, Physiological

KW - Abortion, Spontaneous/metabolism/pathology

KW - Mice, Inbred CBA

KW - Placenta/metabolism/pathology

KW - Vascular Cell Adhesion Molecule-1/biosynthesis

KW - Animals

KW - Male

KW - Female

KW - Mice

KW - Mice, Inbred BALB C

KW - Pregnancy

KW - Gene Expression Regulation

KW - Stress, Physiological

KW - Abortion, Spontaneous/metabolism/pathology

KW - Mice, Inbred CBA

KW - Placenta/metabolism/pathology

KW - Vascular Cell Adhesion Molecule-1/biosynthesis

U2 - 10.1016/j.jri.2011.01.021

DO - 10.1016/j.jri.2011.01.021

M3 - SCORING: Journal article

VL - 89

SP - 207

EP - 211

JO - J REPROD IMMUNOL

JF - J REPROD IMMUNOL

SN - 0165-0378

IS - 2

M1 - 2

ER -