Differential Expression in Endometriosis Tissue versus Endometrium of the Uterine Adenogenesis Factors PRL-R, GH, IGF1, and IGF2

Endometriosis is characterized by the presence of endometrial glandular and stromal structures outside the uterine cavity. It is an inflammatory estrogen dependent disease characterized by gene polymorphisms. This is a very frequent pathology and represents one of the most important causes of infertility, as well as having an important level of morbidity in patients. Recently, an alteration of the processes of organogenesis of the uterus has been proposed as a pathogenetic mechanism of endometriosis. In this article we have compared the expression in deep endometriotic lesions and in normal endometrial tissue of some of the molecular factors known to be involved in the embryonic development of the uterine glands. In detail, we found by immunohistochemistry a significant higher expression both for epithelium and stroma in the controls respect to the endometriosis samples for insulin growth factor 1 (IGF1) and IGF2, whereas for the prolactin receptor (PRL-R), this result was detected only for the epithelium. On the other hand, we found for growth hormone (GH) a significant higher expression in the epithelium of endometriosis samples respect to the controls. The correlation data generated can give indications on some of the molecular mechanisms responsible for the adenogenesis and survival of endometriosis structures outside of the uterus.

Automated summary

Endometriosis is a common disease characterized by the presence of endometrial tissue outside the uterus. It is estrogen dependent and has significant impacts on fertility and patient morbidity. Studies suggest that altered uterine organogenesis may contribute to the development of endometriosis. This article compared the expression of molecular factors involved in embryonic development between deep endometriotic lesions and normal endometrial tissue, and found differences in the expression of insulin growth factor, prolactin receptor, and growth hormone.