通过对SOX9表达的升调,EGR1促进卵巢过度刺激综合征
Huihui Wang1, Weijia Chen2, Yinan Huang3
1Department of Obstetrics and Gynecology, Center for Reproductive Medicine, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine; The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
早期生长反应蛋白1 (EGR1) 通过上调SOX9和血管内皮生长因子 (VEGF) 来促进卵巢过度刺激综合征 (OHSS) 的进展. 多巴胺治疗通过抑制EGR1/SOX9通路改善OHSS,提供潜在的治疗点.
科学领域:
- 生殖内分泌学 生殖内分泌学
- 分子生物学分子生物学
- 在瘤学瘤学.
背景情况:
- 血管新生是卵巢过度刺激综合征 (OHSS) 发展的关键因素.
- 早期生长反应蛋白1 (EGR1) 与血管生成有关,可能在OHSS中发挥作用.
研究的目的:
- 研究EGR1在OHSS进展中的作用和机制.
- 探索多巴胺作为OHSS治疗剂的潜力.
主要方法:
- 用RNA测序来识别差异表达的基因.
- 在体外 (KGN细胞) 和体内 (小鼠) 的OHSS模型.
- 定量实时PCR,西斑,ELISA,光酶记者测定和染色体免疫沉以评估基因和蛋白质表达和相互作用.
主要成果:
- 在OHSS患者和OHSS小鼠模型的颗粒细胞中,EGR1和SOX9的高调显著.
- 人体胆性腺激素 (hCG) 治疗增加了KGN细胞中的VEGF,EGR1和SOX9水平;EGR1沉默逆转了这些影响.
- 通过其促进体,EGR1直接调节SOX9的表达.
- 多巴胺的使用减少了hCG诱导的VEGF,改善了小鼠的OHSS,并降低了EGR1和SOX9的表达.
结论:
- 通过调节SOX9和VEGF,EGR1促进OHSS的进展.
- 多巴胺通过抑制EGR1/SOX9通路对OHSS产生保护作用.
- EGR1/SOX9级联是OHSS治疗的潜在治疗标.
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