子宫内膜异位症（内异症）是妇科领域的常见病及难治病，目前发病机制尚不明确。前期研究发现内异症在位内膜MAT2A基因高表达促进原代子宫内膜细胞增殖、侵袭及转移，抑制细胞凋亡，提示MAT2A可能是导致子宫内膜细胞异位种植生长的重要基因。已知大鼠MAT2A基因启动子区中存在PPREs与过氧化物酶体增殖物激活受体γ（PPARγ）相互作用，调节细胞静止/激活状态。预实验研究表明内异症在位内膜组织与细胞中，PPARγ与MAT2A表达呈负相关，据此我们推测PPARγ在内异症中的作用也是通过调节MAT2A基因的表达来实现的。本研究旨在鉴定子宫内膜细胞MAT2A基因启动子区中是否存在PPREs及PPARγ与每个PPRE区域的结合效率，检测PPARγ是否通过调控MAT2A转录活性进而影响子宫内膜细胞功能，探讨内异症在位内膜MAT2A基因表达增高的分子机制，为寻找新的内异症诊断标志物及基因治疗靶点提供理论依据。

Endometriosis(EMs) is one of the most commonly encountered benign gynecological disorders. Up to now, the etiology and pathogenesis of endometriosis are not clear. In previous study, we found that overexpression of MAT2A in eutopic endometrium of endometriosis was associated with enhanced cell proliferation, invasion, and reduced apoptosis. It provided the initial evidence that overexpression of MAT2A facilitated the formation of ectopic lesions and played an important role in the development of endometriosis. Peroxisome proliferator-activated receptor typeγ(PPARγ) is an essential transcription factor. It was reported that PPARγ exerted a strong, negative regulatory control on MAT2A transcription by binding to PPAR response elements (PPREs) in the MAT2A promoter of quiescent hepatic stellate cells (HSCs). Our previous data showed that silencing PPARγ increased MAT2A transcription in normal endometrium whereas over-expressing it had the opposite effect in the eutopic endometrium of endometriosis, which demonstrated that PPARγ may exert its biological effects in the pathogenesis of endometriosis by negatively controlling MAT2A gene. Our present studies plan to detect mRNA and protein levels of MAT2A and PPARγ between the eutopic endometrium of endometriosis and controls and analyze the correlation of their expression. Meanwhile, we identify PPREs in the MAT2A promoter of endometrial stromal cells, examine the binding of PPARγ to each PPRE sites on the MAT2A promoter, and discuss that whether PPARγ effects the biological characteristics of the endometrium by regulating the MAT2A transcriptional activity.We first investigate the the molecular mechanism responsible for the transcriptional regulation of the MAT2A gene in endometriosis, which provide a wider perspective for understanding the pathogenesis of endometriosis and offer the basis for molecular-targeted diagnosis and therapy of endometriosis.