image: Regulatory hierarchy between KLF12 overexpression and pregnancy outcomes
Credit: SHI Qingqing; WU Xing; KANG Nannan; ZHOU Jidong; ZHEN Xin; LI Zewu; YAN Guijun; SUN Haixiang; LIU Jingyu; LIU Yang
Miscarriages affect approximately 15% of recognized pregnancies, with placental dysfunction identified as a major contributing factor. A study published in Reproductive and Developmental Medicine uncovered a critical link between elevated levels of the Kruppel-like factor 12 (KLF12) protein and impaired placental development, shedding light to the causes of unexplained miscarriages.
The research team analyzed placental tissue samples from women with normal pregnancies and those who had experienced unexplained miscarriages. They found significantly higher levels of KLF12 in the miscarriage group.
Using a laboratory model of placental development with BeWo cells, researchers observed that KLF12 expression naturally decreases during normal placental development, but when levels remained elevated, it directly inhibited the expression of GCM1, a critical gene for placental cell fusion.
KLF12 could serve as a biomarker for identifying women at higher risk of miscarriage. "If we can develop strategies to normalize KLF12 levels or counteract its effects on GCM1, we might be able to improve placental function and reduce miscarriage rates.", says the corresponding author.
This research deepens our understanding of KLF12's role in pregnancy and provides a promising direction for developing targeted treatments to support placental health and improve pregnancy outcomes.
The research team plans to expand their work to identify specific triggers that lead to KLF12 overexpression. "This is just the beginning," says the author. "Our next steps is to explore how factors like stress, inflammation, and environmental toxins might influence KLF12 levels during pregnancy."
Journal
Reproductive and Developmental Medicine
Method of Research
Experimental study
Article Title
Elevated levels of KLF12 impair trophoblast syncytialization via GCM1 downregulation
Article Publication Date
29-Jul-2024