lncRNA 9708-1：雌激素在阴道黏膜感染与防御中的新机制

阴道感染是妇科最常见疾病，雌激素为其关键影响因素。lncRNA 9708-1是我们利用芯片发现的一条在围绝经期（低雌激素）女性阴道上皮组织显著低表达的功能未知的lncRNA。实验发现lncRNA 9708-1过表达可使阴道上皮细胞迁移能力增强、黏附能力减弱；软件预测FAK为其靶基因；而雌激素能诱导lncRNA 9708-1表达，致FAK增高，降低细胞黏附、促进其迁移/脱落，提示雌激素可能通过lncRNA 9708-1/FAK机制调控阴道上皮的黏附/迁移而参与阴道内稳态的维持及防御。本研究拟从正反两方面论证雌激素经lncRNA 9708-1调控阴道上皮细胞的黏附/迁移及其对雌激素的应答；以FAK为线索，揭示lncRNA 9708-1的分子机制。本课题拟阐明雌激素在阴道黏膜感染与防御中的未知机制，补充阴道感染发病理论，为复杂的阴道感染提供潜在、共性的干预靶标，具有源头创新性。

Vaginal infection is the most common gynecological disease, and estrogen is key influence factor. lncRNA 9708-1 was an unknown lncRNA with significant low expression screened from menopausal woman’s (low estrogen) vaginal epithelial tissue through chip. The preliminary experiment found that lncRNA 9708-1 overexpression was able to strengthen cell migration ability and weaken adhesion ability, and software forecasted that FAK was its target gene. Since it was able to induce lncRNA 9708-1 expression, caused FAK increasing, reduced cell adhesion, and promoted its migration/dropping, estrogen may regulate the adhesion/ migration of vaginal epithelial cells, resulted in participating in the vaginal homeostasis maintenance and defense through lncRNA 9708-1/FAK mechanism. Such research aims to comprehensively demonstrate the estrogen response characteristics and functions of lncRNA 9708-1, taking FAK as the clue to reveal the functional mechanism of lncRNA 9708-1. The present research is helpful to illuminate estrogen’s unknown mechanism in vaginal mucosa infection and defense, supplement vaginal infection pathogenic theory, provide potential common intervention targets for complicated vaginal infection, which has revolutionary innovation.