Identification of the primary outcomes that result from deficient spiral arterial modification in pregnant mice

被引:32
作者
Croy, B. Anne [1 ]
Burke, Suzanne D. [1 ]
Barrette, Valerie F. [1 ]
Zhang, Jianhong [1 ]
Hatta, Kota [2 ]
Smith, Graeme N. [3 ]
Bianco, Juares [1 ,5 ]
Yamada, Aureo T. [5 ]
Adams, Michael A. [4 ]
机构
[1] Queens Univ, Dept Anat & Cell Biol, Kingston, ON K7L 3N6, Canada
[2] Queens Univ, Dept Microbiol & Immunol, Kingston, ON K7L 3N6, Canada
[3] Queens Univ, Dept Obstet & Gynecol, Kingston, ON K7L 3N6, Canada
[4] Queens Univ, Dept Pharmacol & Toxicol, Kingston, ON K7L 3N6, Canada
[5] Univ Estadual Campinas, Inst Biol, Lab Histochem & Cytochem, Campinas, SP, Brazil
基金
加拿大自然科学与工程研究理事会;
关键词
Fecundity; Immune system; Mean arterial pressure; Placental growth; Vascular remodeling; NATURAL-KILLER-CELLS; TROPHOBLAST INVASION; PLACENTAL GROWTH; INTERFERON-GAMMA; T-CELL; PREECLAMPSIA; RISK; EXPRESSION; DISEASE;
D O I
10.1016/j.preghy.2010.10.002
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Pre-eclampsia, an acute complication of human pregnancy, is associated with incomplete physiological modification of decidual spiral arteries. This is thought to promote oxidative stress from perfusion/reperfusion of the placenta and to restrict placental and fetal growth. Alymphoid (genotype Rag2 (/) /Il2rg (/)) mice, sufficient in dendritic and myeloid cell functions, lack spiral arterial modification with individual spiral arteries having similar to 1.7 x the vascular resistance and 0.66 x the blood velocity of +/+ mice. Their placentae are not measurably hypoxic and neither placental growth nor fetal survival is impaired and gestational hypertension is not seen. Thus, lymphocytes rather than vascular adaptations appear to be the pivotal contributors to the clinical complications of pre-eclampsia. (C) 2010 International Society for the Study of Hypertension in Pregnancy. Published by Elsevier B.V. All rights reserved
引用
收藏
页码:87 / 94
页数:8
相关论文
共 43 条
[1]   Interferon γ contributes to initiation of uterine vascular modification, decidual integrity, and uterine natural killer cell maturation during normal murine pregnancy [J].
Ashkar, AA ;
Di Santo, JP ;
Croy, BA .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 192 (02) :259-269
[2]   Uric acid attenuates trophoblast invasion and integration into endothelial cell monolayers [J].
Bainbridge, Shannon A. ;
Roberts, James M. ;
von Versen-Hoynck, Frauke ;
Koch, Jessa ;
Edmunds, Lia ;
Hubel, Carl A. .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2009, 297 (02) :C440-C450
[3]   Spiral Arterial Remodeling Is Not Essential for Normal Blood Pressure Regulation in Pregnant Mice [J].
Burke, Suzanne D. ;
Barrette, Valerie F. ;
Bianco, Juares ;
Thorne, Julie G. ;
Yamada, Aureo T. ;
Pang, Stephen C. ;
Adams, Michael A. ;
Croy, B. Anne .
HYPERTENSION, 2010, 55 (03) :729-737
[4]   Placental oxidative stress: From miscarriage to preeclampsia [J].
Burton, GJ ;
Jauniaux, E .
JOURNAL OF THE SOCIETY FOR GYNECOLOGIC INVESTIGATION, 2004, 11 (06) :342-352
[5]  
BUZAS EI, 1993, CLIN EXP IMMUNOL, V94, P252
[6]   LYMPHOID DEVELOPMENT IN MICE WITH A TARGETED DELETION OF THE INTERLEUKIN-2 RECEPTOR-GAMMA CHAIN [J].
DISANTO, JP ;
MULLER, W ;
GUYGRAND, D ;
FISCHER, A ;
RAJEWSKY, K .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (02) :377-381
[7]   Altered Global Gene Expression in First Trimester Placentas of Women Destined to Develop Preeclampsia [J].
Founds, S. A. ;
Conley, Y. P. ;
Lyons-Weiler, J. F. ;
Jeyabalan, A. ;
Hogge, W. Allen ;
Conrad, K. R. .
PLACENTA, 2009, 30 (01) :15-24
[8]   Emerging concepts in preeclampsia investigation [J].
Gammill, Hilary S. ;
Roberts, James M. .
FRONTIERS IN BIOSCIENCE-LANDMARK, 2007, 12 :2403-2411
[9]   Systemic inflammatory priming in normal pregnancy and preeclampsia: The role of circulating syncytiotrophoblast microparticles [J].
Germain, Sarah J. ;
Sacks, Gavin P. ;
Soorana, Suren R. ;
Sargent, Ian L. ;
Redman, Christopher W. .
JOURNAL OF IMMUNOLOGY, 2007, 178 (09) :5949-5956
[10]   Ultrastructural studies of implantation sites from mice deficient in uterine natural killer cells [J].
Greenwood, JD ;
Minhas, K ;
Di Santo, JP ;
Makita, M ;
Kiso, Y ;
Croy, BA .
PLACENTA, 2000, 21 (07) :693-702