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The role of estrogen in the pathophysiology of tubal ectopic pregnancy

Journal article
Authors Linus Ruijin Shao
Yi Feng
S. E. Zou
Birgitta Weijdegård
G. C. Wu
Mats Brännström
Håkan Billig
Published in American Journal of Translational Research
Volume 4
Issue 3
Pages 269-278
ISSN 1943-8141
Publication year 2012
Published at Institute of Neuroscience and Physiology, Department of Physiology
Institute of Clinical Sciences, Department of Obstetrics and Gynecology
Pages 269-278
Language en
Links www.ajtr.org/files/AJTR1206002.pdf
Keywords 17 beta-estradiol, estrogen receptor subtypes, human, infertility, tubal ectopic pregnancy, ciliary beat frequency, human fallopian-tube, female reproductive organ, in-situ hybridization, natural-killer-cells, beta messenger-rnas, receptor-alpha, insulin-like, rat oviduct, knockout mouse, rcelledo ml, 1986, endocrinology, v119, p1189
Subject categories Obstetrics and gynaecology

Abstract

17β-estradiol, acting through estrogen receptors α and β, plays a fundamental role in the regulation of Fallopian tube cell homeostasis and in the modulation of normal tubal physiological processes. Fluctuations in E2 levels also play crucial roles in the initiation or progression of numerous human diseases. Fallopian tube malfunction often results in tubal ectopic pregnancy, which is one cause of maternal morbidity and mortality in women. Several factors have been proposed to be associated with increased risk of tubal ectopic pregnancy, but whether these factors are the cause of, or are merely symptoms of, such pregnancies remains unresolved due to the lack of knowledge in regards to the mechanisms by which embryos inadvertently implant in the Fallopian tube. This review summarizes recent findings, including data from our own laboratory, on E2 metabolism and estrogen receptor (ER) subtype expression within the Fallopian tube in humans and rodents. This review also outlines several important, unresolved questions in the field that, once addressed, could offer important clues into how E2/ER signaling contributes to the pathology of tubal function. A better understanding of the specific functions of estrogen receptor subtypes in vivo, as well as of the mechanism and consequences of receptor subtype interactions is critical to understanding their respective roles in Fallopian tube physiology and in the pathophysiology and etiology of tubal ectopic pregnancy.

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