کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5622175 | 1579191 | 2017 | 7 صفحه PDF | دانلود رایگان |
- The expression of TFPI-2 was significantly elevated in PE placentas when compared with those in NP ones.
- Hypomethylation of the TFPI-2 promoter was detected in the placentas, with a significant decrease in the PE ones.
- The methylation level was significantly decreased at CpG_6, CpG_15 and CpG_18.19 in PE patients than that in NP ones.
- Epigenetic mechanism might contribute to the pathogenesis of PE.
ObjectivesTo investigate the expression, DNA methylation status and its regulatory mechanism of tissue factor pathway inhibitor 2 (TFPI-2) in human placenta tissues of preeclampsia (PE).Material and methodsWe studied the mRNA and protein expression and the promoter methylation levels of TFPI-2 in the PE placentas compared with those in the normal pregnant (NP) women. Quantitative real-time polymerase chain reaction, immunohistochemistry, western blot, and Sequenom MassARRAY were used for placenta tissue detection.ResultsThe expressions of TFPI-2 mRNA and protein were significantly elevated in the PE placentas when compared with those in the NP ones (P < 0.05). Hypomethylation of the TFPI-2 promoter was detected both in PE patients and NP women, with a significant decrease in PE placentas (P = 0.005). The methylation level was significantly decreased at CpG_6 (â 168 to â 167), CpG_15 (â 98 to â 97) and CpG_18.19 (â 68 to â 65) in PE patients than that in normal placentas (P < 0.05). However, the expression of DNMT-1 didn't show significant difference between the two groups (P > 0.05).ConclusionOver-expression of TFPI-2 and aberrant promoter mythylation status presented in the PE placentas, suggesting that epigenetic mechanism might contribute to the pathogenesis of PE.
Journal: Thrombosis Research - Volume 152, April 2017, Pages 7-13