Hereditas · 2025
HOXA13 promotes high glucose-induced trophoblast cell growth and migration during gestational diabetes by regulating the smad2 pathway.
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Zhao Fei, Liu Xinhong, Qin Hong
Аннотация
BACKGROUND: Gestational diabetes mellitus (GDM) is considered the most common complication of pregnancy, and is a very dangerous disease for both mother and baby. Homeobox A13 (HOXA13) has been discovered to join into some diseases through exhibiting regulatory functions. Importantly, hypermethylation of HOXA13 has been observed in the placental tissues of preeclampsia. However, the regulatory impacts of HOXA13 on GDM progression keep dimness.
METHODS: The GDM cell model and GDM rat model were established. The expressions of genes were measured through RT-qPCR, western blot or IHC assay. The cell proliferation was tested through MTT and Edu assays. The cell migration was determined through Transwell assay. The fasting blood glucose of rats was detected through the blood glucose meter.
RESULTS: HOXA13 was verified to be lowly expressed in placental tissues from GDM patients. In addition, the cell proliferation and migration abilities of trophoblast cells were attenuated after high glucose (HG) treatment, but these impacts were counteracted after HOXA13 overexpression. It was further demonstrated that HOXA13 affected the proliferation and migration abilities of HG-triggered trophoblast cells by enhancing smad2 expression. At last, it was testified that HOXA13 can ameliorate GDM symptoms in vivo.
CONCLUSION: This study manifested that HOXA13 accelerated HG-triggered trophoblast cell growth and migration by regulating the smad2 pathway. This discovery hinted that HOXA13 may be a target for ameliorating GDM.
METHODS: The GDM cell model and GDM rat model were established. The expressions of genes were measured through RT-qPCR, western blot or IHC assay. The cell proliferation was tested through MTT and Edu assays. The cell migration was determined through Transwell assay. The fasting blood glucose of rats was detected through the blood glucose meter.
RESULTS: HOXA13 was verified to be lowly expressed in placental tissues from GDM patients. In addition, the cell proliferation and migration abilities of trophoblast cells were attenuated after high glucose (HG) treatment, but these impacts were counteracted after HOXA13 overexpression. It was further demonstrated that HOXA13 affected the proliferation and migration abilities of HG-triggered trophoblast cells by enhancing smad2 expression. At last, it was testified that HOXA13 can ameliorate GDM symptoms in vivo.
CONCLUSION: This study manifested that HOXA13 accelerated HG-triggered trophoblast cell growth and migration by regulating the smad2 pathway. This discovery hinted that HOXA13 may be a target for ameliorating GDM.