Dissecting the miR-451a-Mif Pathway in Endometriosis Pathophysiology Using a Syngeneic Mouse Model: Temporal Expression of Lesion Mif Receptors, Cd74 and Cxcr4.
Dissecting the miR-451a-Mif Pathway in Endometriosis Pathophysiology Using a Syngeneic Mouse Model: Temporal Expression of Lesion Mif Receptors, Cd74 and Cxcr4.
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DOI：
10.3390/biomedicines10071699
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发表时间：
2022-07-14
期刊：
影响因子：
4.7
通讯作者：
中科院分区：
文献类型：
--
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子宫内膜异位症是一种以疼痛和不孕为特征的神秘疾病，其子宫内膜组织生长在异位部位，主要是盆腔。子宫内膜异位症的发病机制和病理生理学是复杂的，并假定涉及炎症，细胞增殖和转录后调控途径等的改变。我们对子宫内膜异位症的发病机制和病理生理学的理解是进一步复杂的事实，子宫内膜异位症只能通过腹腔镜诊断后，疾病已经表现出来。这使得很难理解真正的发病机制，因为因果关系很难确定。为了帮助我们了解子宫内膜异位症的发病机制和病理生理学，已经开发了许多啮齿动物模型。在这种情况下，我们讨论了进一步评估的miR-451 a-巨噬细胞迁移抑制因子（Mif）途径，有助于病变的生存。具体而言，我们评估的时间表达病变的Mif受体，Cd 74和Cxcr 4使用宿主小鼠表达野生型或miR-451 a缺陷病变。与在人类和非人灵长类动物子宫内膜异位症模型中观察到的相似，Cd 74表达在病变组织中以时间方式升高，而Cxcr 4的表达在初始病变建立期间显示出最小的增加，但在寿命后期降低。在初始病变建立期间，miR-451 a的缺失与Cd 74的增加相关，但与Cxcr 4的表达无关。本研究获得的数据进一步支持了Mif受体、Cd 74和Cxcr 4在子宫内膜异位症病理生理学中的作用。
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 miR-451a—macrophage migration inhibitory factor (Mif) pathway which contributes to lesion survival. Specifically, we evaluate the temporal expression of lesion Mif receptors, Cd74 and Cxcr4 using host mice which express wild-type or miR-451a deficient lesions. Similar to that observed in humans and a non-human primate model of endometriosis, Cd74 expression is elevated in lesion tissue in a temporal fashion while that of Cxcr4 shows minimal increase during initial lesion establishment but is reduced later during the lifespan. Absence of miR-451a during initial lesion establishment is associated with an augmentation of Cd74, but no Cxcr4 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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影响因子：
2.9
作者：
Moridi, Irene;Mamillapalli, Ramanaiah;Taylor, Hugh S.
通讯作者：
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