1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Reprod Sci. 2014 Jan;21(1):72-81. doi: 10.1177/1933719113488448. Epub 2013 May 23.
Krüppel-like factor 8 (KLF8) is a pivotal transcription factor expressed in the human placenta that can regulate cell invasion. The objective of this study was to assess whether a hypoxia-reoxygenation (H/R) environment affects placental KLF8 expression levels and subcellular localization and to evaluate the relationship between KLF8 levels and trophoblast invasion activity. Human first trimester villous tissues from normal pregnancies and third trimester placentas from pregnancies with or without preeclampsia (PE) were used for the detection of KLF8 expression and correlating its levels with metalloproteinase 9 (MMP-9) expression. In addition, HTR8/SVneo cells were used to mimic the effects of an H/R environment on placentas to study KLF8 expression and trophoblast invasion. The KLF8 levels, MMP-9 levels, and trophoblast invasion were similarly altered; the levels peaked at 8 to 10 weeks of gestation and declined thereafter along with oxygen tension increased from hypoxia to normoxia during early pregnancy, decreased in third trimester placentas from PE pregnancies featured by repeated H/R and HTR8/SVneo cells exposed to H/R compared with the control. Moreover, a visible reduction in KLF8 immunoreactivity was present in the nuclei of cytotrophoblast cells in human villous tissues at 11 weeks, and partial cytoplasmic accumulation of KLF8 was observed in HTR8/SVneo cells treated with H/R. In conclusion, these findings strongly suggest that H/R reduces the expression and nuclear localization of KLF8 to inhibit the trophoblast invasion by downregulating MMP-9 levels. The KLF8 may play a vital role in the pathogenesis of PE as a novel oxygen tension sensor.
Krüppel 样因子 8(KLF8)是一种在人胎盘组织中表达的关键转录因子,可调节细胞侵袭。本研究旨在评估缺氧/复氧(H/R)环境是否影响胎盘组织中 KLF8 的表达水平及其亚细胞定位,并评估 KLF8 水平与滋养细胞侵袭活性之间的关系。本研究采用正常妊娠和子痫前期(PE)妊娠的人早孕绒毛组织和足月胎盘组织检测 KLF8 的表达,并将其水平与金属蛋白酶 9(MMP-9)的表达相关联。此外,采用 HTR8/SVneo 细胞模拟 H/R 环境对胎盘的影响,以研究 KLF8 的表达和滋养细胞侵袭。结果发现,KLF8 水平、MMP-9 水平和滋养细胞侵袭活性均发生相似的改变;在妊娠早期,随着氧分压从低氧向常氧增加,KLF8 水平在妊娠 8 至 10 周时达到峰值,此后逐渐下降;与对照组相比,PE 妊娠的足月胎盘组织和暴露于 H/R 的 HTR8/SVneo 细胞中的 KLF8 水平下降。此外,在 11 周的人绒毛组织中,可见细胞质中的 KLF8 免疫反应性明显减少,并且在接受 H/R 处理的 HTR8/SVneo 细胞中观察到 KLF8 的部分细胞质积累。总之,这些发现强烈表明,H/R 通过下调 MMP-9 水平降低了 KLF8 的表达和核定位,从而抑制了滋养细胞的侵袭。KLF8 可能作为一种新型的氧张力传感器,在 PE 的发病机制中发挥重要作用。