Endometriotic Cells Exhibit Metaplastic Change and Oxidative DNA Damage as Well as Decreased Function,Compared to Normal Endometrium |
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Authors: | Email author" target="_blank">M?SlaterEmail author G?Quagliotto M?Cooper CR?Murphy |
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Institution: | (1) Anatomy and Histology, School of Medical Sciences, The University of Sydney, Anderson Stuart Building F13, 2006, NSW, Australia;(2) Department of Anatomical Pathology, Royal Prince Alfred Hospital, Sydney, NSW, Australia;(3) Department of Endoscopic Surgery, King George V Hospital, Sydney, NSW, Australia |
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Abstract: | Summary A widely accepted theory of the etiology of endometriosis is that it originates from the implantation and invasion of cells
from retrograde menstruation to various sites in the body particularly the pelvic peritoneal cavity. Little is known of the
function of these cells in ectopic sites. Normal endometrium was compared with endometriotic tissue using an antibody to Placental
Cadherin (P Cadherin), a recently studied cadherin that is implicated in metaplasia and early neoplasia and also 8-hydroxyguanine,
an indicator of oxidative DNA damage. Comparisons of endometrial tissue function were made using expression of transforming
growth factor β-1 (TGFβ-1) and insulin-like growth factor-I (IGF-I). There was no labelling for anti-P Cadherin or anti-8-hydroxydeoxyguanosine
in normal endometrium but marked labelling for both on the apical surface of the endometriotic epithelium. Studies of markers
of normal endometrial function were all de-expressed in endometriosis. This study indicates that endometriosis cells are abnormal
and exhibit oxidative DNA damage, metaplasia and markedly reduced function compared to normal endometrium. |
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