| Summary: | Endometriosis is an enigmatic disease characterized by pain and infertility in which endometrial tissue grows in ectopic locations, predominantly the pelvic cavity. The pathogenesis and pathophysiology of endometriosis is complex and postulated to involve alterations in inflammatory, cell proliferation and post-transcriptional regulatory pathways among others. Our understanding on the pathogenesis and pathophysiology of endometriosis is further complicated by the fact that endometriosis can only be diagnosed by laparoscopy only after the disease has manifested. This makes it difficult to understand the true pathogenesis as a cause-and-effect relationship is difficult to ascertain. To aid in our understanding on endometriosis pathogenesis and pathophysiology, numerous rodent models have been developed. In this case, we discuss further assessment of a <i>miR-451a</i>—macrophage migration inhibitory factor (Mif) pathway which contributes to lesion survival. Specifically, we evaluate the temporal expression of lesion Mif receptors, <i>Cd74</i> and <i>Cxcr4</i> using host mice which express wild-type or <i>miR-451a</i> deficient lesions. Similar to that observed in humans and a non-human primate model of endometriosis, <i>Cd74</i> expression is elevated in lesion tissue in a temporal fashion while that of <i>Cxcr4</i> shows minimal increase during initial lesion establishment but is reduced later during the lifespan. Absence of <i>miR-451a</i> during initial lesion establishment is associated with an augmentation of <i>Cd74</i>, but no <i>Cxcr4</i> expression. The data obtained in this study provide further support for a role of Mif receptors, Cd74 and Cxcr4 in the pathophysiology of endometriosis.
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