希斯酸乳化通过向子宫内膜异位症中的HMGB1促进细胞增殖,迁移和入侵
Jie Chen1, Pengfei Qin1, Yanli Sun1
1Department of Obstetrics and Gynecology, Women's Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, Nanjing, Jiangsu 210004, China.
Journal of biomedical research
|November 9, 2023
概括
乳酸酸促进子宫内膜异位症的进展,通过增加基因素乳酸和高流动性组框1 (HMGB1) 的表达. 这一发现为子宫内膜异位症治疗提供了潜在的新目标.
科学领域:
- 生物化学 生物化学
- 细胞生物学 细胞生物学
- 妇科 妇科医生 妇科
背景情况:
- 子宫内膜异位症涉及子宫外的子宫内膜状组织,但其机制尚不清楚.
- 蛋白质的乳酸修饰,称为乳酸化,是最近的一个研究领域.
- 在子宫内膜异位症的背景下,基因组乳酸化,特别是H3K18lac,尚未得到广泛的研究.
研究的目的:
- 为了研究乳酸和基因素乳化在子宫内膜异位症进展中的作用.
- 探索乳酸,乳糖和子宫内膜异位症相关的细胞行为之间的机械联系.
- 根据乳酸代谢来确定子宫内膜异位症的潜在治疗点.
主要方法:
- 在子宫外和正常子宫内膜组织和细胞中,乳酸盐含量和素H3 lysine 18乳化 (H3K18lac) 的比较分析.
- 在子宫内膜异位症模型中评估乳酸对细胞增殖,迁移和侵入的影响.
- 调查高流动性组框1 (HMGB1) 和AKT信号在调解乳酸的作用中的作用.
主要成果:
- 乳酸和乳酸脱酶A水平升高与子宫外子宫内膜组织和细胞中H3K18lac增加相关.
- 乳酸盐显著增强了子宫内膜异位症细胞的增殖,迁移和入侵.
- 乳酸诱导的H3K18lac提高了HMGB1的表达,通过AKT酸化促进细胞行为;HMGB1的淘汰扭转了这些效应.
结论:
- 乳酸盐通过基因素乳化促进子宫内膜异位症的进展,特别是H3K18lac.
- 通过乳酸诱导的乳化对HMGB1的升级是驱动子宫内膜异位症的关键机制.
- 向乳酸代谢和HMGB1可能为子宫内膜异位症提供新的治疗策略.
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