Abstract

PurposeDeep infiltrating endometriosis (DIE) is defined as an endometriotic lesion penetrating to a depth of >5 mm and is associated with pelvic pain, but the underlying mechanisms are unclear. Our objective is to investigate whether plasminogen activator inhibitor-1 expression (PAI-1) in endometriotic tissues is increased in women with DIE.MethodsIn this blinded in vitro study, immunohistochemistry and Histoscore were used to examine the expression of PAI-1 in glandular epithelium (GECs) and stroma (SCs) in a total of 62 women: deep infiltrating uterosacral/rectovaginal endometriosis (DIE; n = 13), ovarian endometrioma (OMA; n = 14), superficial peritoneal uterosacral/cul-de-sac endometriosis (SUP; n = 23), uterine (eutopic) endometrium from women with endometriosis (UE; n = 6), and non-endometriosis eutopic endometrium (UC; n = 6). The following patient characteristics were also collected: age, American Fertility Society stage, hormonal suppression, phase of menstrual cycle, dysmenorrhea score and deep dyspareunia score.ResultsPAI-1 expression in GECs and SCs of the DIE group was significantly higher than that of SUP group (p = 0.01, p = 0.01, respectively) and UE group (p = 0.03, p = 0.04, respectively). Interestingly, increased PAI-1 expression in GECs and SCs was also significantly correlated with increased dysmenorrhea (r = 0.38, p = 0.01; r = 0.34, p = 0.02, respectively).ConclusionsWe found higher expression of PAI-1 in DIE, and an association between PAI-1 and worse dysmenorrhea.

Highlights

  • Endometriosis is a common, estrogen-dependent, chronic gynecological disorder associated with pelvic pain and infertility

  • Increased Plasminogen activator inhibitor-1 (PAI-1) expression in glandular epithelial cells (GECs) and stroma cells (SCs) was significantly correlated with increased dysmenorrhea (r = 0.38, p = 0.01; r = 0.34, p = 0.02, respectively)

  • We found higher expression of PAI-1 in deep infiltrating endometriosis (DIE), and an association between PAI-1 and worse dysmenorrhea

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Summary

Introduction

Endometriosis is a common, estrogen-dependent, chronic gynecological disorder associated with pelvic pain and infertility. It is characterized by the presence of uterine endometrial tissue (glandular epithelium and stroma) outside of its normal location—mainly on the pelvic peritoneum, and on the ovaries and other pelvic organs, and more rarely in the pericardium, pleura, and even the brain [1, 2, 3]. The plasminogen activator (PA) system has been implicated in tumor invasion, compromising anatomical barriers and regulating the migration of tumor cells into adjacent normal tissues. Liu et al [5] investigated the importance of the urokinase-type plasminogen activator (u-PA) system and PAI-1 in human lung cancer cell invasion. The expression of PAI-1 was found to be significantly higher in women with stage III endometrial cancer compared to women with stage I or II [9]

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