Lu Huixia, Li Shaobo, Wu Qi
Clinical Medical College of Dali University, Dali, Yunnan, China.
The First Affiliated Hospital of Dali University, Dali, 671000, Yunnan, China.
Arch Gynecol Obstet. 2018 Jan;297(1):93-99. doi: 10.1007/s00404-017-4549-8. Epub 2017 Oct 24.
To elucidate the role of retinoic acid (RA) in autophagy-mediated endometriosis.
The mRNA and protein expressions of autophagy markers were examined in Ishikawa cells and endometriotic stromal cells (ESCs) after RA treatment. Beclin1 expression was specifically analyzed in clinical samples of endometriosis. The effect of Beclin1 knockdown on ESC growth was assessed, and the effect of autophagy inhibition on the sensitivity of endometriotic cells to RA was analyzed.
RA treatment enhanced the autophagy in ESCs, and Beclin1 expression showed a negative correlation with the clinical stage of endometriosis. Beclin1 knockdown enhanced ESC growth, whereas RA treatment reversed this effect. Furthermore, inhibition of autophagy by chloroquine (CQ) and Beclin1 knockdown did not show any positive effect on the sensitivity of endometriotic cells to RA.
RA treatment induces autophagy and Beclin1 may play an important role in endometriosis progression.
阐明视黄酸（RA）在自噬介导的子宫内膜异位症中的作用。
在RA处理后的 Ishikawa 细胞和子宫内膜异位症间质细胞（ESC）中检测自噬标志物的 mRNA 和蛋白质表达。在子宫内膜异位症临床样本中特异性分析 Beclin1 的表达。评估 Beclin1 敲低对 ESC 生长的影响，并分析自噬抑制对子宫内膜异位症细胞对 RA 敏感性的影响。
RA 处理增强了 ESC 中的自噬，且 Beclin1 表达与子宫内膜异位症的临床分期呈负相关。Beclin1 敲低增强了 ESC 的生长，而 RA 处理逆转了这一效应。此外，氯喹（CQ）抑制自噬和 Beclin1 敲低对子宫内膜异位症细胞对 RA 的敏感性均未显示出任何积极作用。
RA治疗诱导自噬，且Beclin1可能在子宫内膜异位症进展中起重要作用。
