Paracrine regulation of endometriotic tissue

Abstract

Endometriosis is a chronic estrogen-dependent gynecological disease, characterized by pelvic pain and infertility, defined as the presence of endometrial glands and stroma within the pelvic peritoneum and other extrauterine sites. In the peritoneal cavity endometrial cells adhere, proliferate and induce an inflammatory response. Despite a long history of clinical and experimental research, the pathogenesis of endometriosis is still controversial. Abnormal immunological activation, the endocrine milieu and the peritoneal environment all dramatically affect endometriotic tissue function. Recent studies suggest that the peritoneal fluid of women with endometriosis contains an increased number of activated macrophages and other immune cells that secrete various local products, such as growth factors and cytokines, which exert a paracrine action on endometriotic cells. Since the peculiar biological characteristics of eutopic endometrium from women with endometriosis differ from endometrium of normal subjects, an important role in the pathogenesis of this complex disease has been suggested. All of these factors contribute to enhanced proliferative and angiogenic activity and a number of functional and structural changes, resulting in the particular behavior of this tissue.

Adenomyosis and infertility

“…Klemmt et al (2006) has now suggested that in women with endometriosis the signalling cascade leading to decidualization might be impaired, potentially decreasing the biochemical maturation required for successful implantation. In addition, women with endometriosis display progesterone resistance (Burney et al, 2007) and their eutopic endometrium shows an impaired decidualization, a fact with important implications for uterine receptivity (Minici et al, 2007(Minici et al, , 2008. The decidualization is associated with an increase in endometrial expression of proteins involved in the suppression of immune cell activity.…”

Steroidogenic Enzyme and Key Decidualization Marker Dysregulation in Endometrial Stromal Cells from Women with Versus Without Endometriosis1

“…It is a major public health problem due to the morbidities associated with accompanying infertility and/or pelvic pain in affected women and an estimated cost for associated healthcare for diagnosis and treatment in 2002 totaling about $22B in the U.S. alone [1]. Infertility in women with endometriosis is believed to be related to the pro-inflammatory milieu in the pelvis affecting oocyte quality, fertilization, and embryo development, and impaired implantation due, in part, to compromised decidualization of endometrial stromal fibroblasts [2, 3]. …”

Modern approaches to endometrial receptivity assessment (a review)

“…-интерлейкина-1, -6, -11 (IL-I, -6, -11) [45,46]; -лейкемияингибирующего фактора (LIF) [47]; -сосудисто-эндотелиального фактора роста (VEGF) [48]; -гепаринсвязывающего эпидермального фак-тора роста (ГС-ЭФР) [49]; -матриксных металлопротеиназ (ММР) и их тканевых ингибиторов (ТIMP) [50]; -интегринов [46,47]; -селектинов [51,52]; -гликоделина A [53]; -кадгеринов [45]; -муцинов [45]; -простагландинов [54]; -белка Ki-67 [55,56]. Перечисленные молекулярные маркеры могут определяться в крови, секрете эндометрия или в са-мой ткани эндометрия, полученной при его биопсии.…”