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The Impact of PTPRK and ROS1 Polymorphisms on the Preeclampsia Risk in Han Chinese Women
Huihui Li1,2,3, Xingyu Yan4, Man Yang5
1Center for Reproductive Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200135, China.
Insights
This study identifies PTPRK as a novel susceptibility gene for preeclampsia (PE) in Han Chinese women. Elevated PTPRK expression in placental tissue is linked to PE, suggesting a potential diagnostic marker.
Area of Science:
- Genetics
- Obstetrics
- Molecular Biology
Background:
- Preeclampsia (PE) is a severe pregnancy complication with unknown etiology, contributing significantly to maternal and infant mortality.
- Genetic factors are increasingly implicated in the development of PE.
- Identifying susceptibility genes is crucial for understanding PE pathogenesis and developing interventions.
Purpose of the Study:
- To identify novel genetic susceptibility factors for preeclampsia (PE).
- To investigate the association of the PTPRK and ROS1 genes with PE risk.
- To examine the expression levels of PTPRK in PE placentas.
Main Methods:
- Human Exome BeadChip assays were performed on 370 PE cases and 482 controls.
- Genotyping of PTPRK and ROS1 was conducted in an independent cohort of 958 PE cases and 1007 controls.
- Immunohistochemistry, qPCR, and Western blotting were used to analyze PTPRK localization and expression in placental tissues.
Main Results:
- The PTPRK rs3190930 allele frequency was significantly different in PE cases compared to controls, especially in severe and early-onset PE subgroups.
- PTPRK protein is localized in placental trophoblast cells.
- Both mRNA and protein levels of PTPRK were significantly elevated in placentas from PE pregnancies.
Conclusions:
- PTPRK is identified as a novel susceptibility gene for preeclampsia in Han Chinese women.
- Increased PTPRK expression in the placenta is associated with preeclampsia.
- The gene ROS1 (rs9489124) showed no significant correlation with PE risk.
Objective:
Preeclampsia (PE) is a severe complication in pregnancy and a leading cause of maternal and infant mortality. However, the exact underlying etiology of PE remains unknown. Emerging evidence indicates that the cause of PE is associated with genetic factors. Therefore, the aim of this study is to identify susceptibility genes to PE.
Materials And Methods:
Human Exome BeadChip assays were conducted using 370 cases and 482 controls and 21 loci were discovered. A further independent set of 958 cases and 1007 controls were recruited for genotyping to determine whether the genes of interest ROS1 and PTPRK are associated with PE. Immunohistochemistry was used for localization. Both qPCR and Western blotting were utilized to investigate the levels of PTPRK in placentas of 20 PE and 20 normal pregnancies.
Results:
The allele frequency of PTPRK rs3190930 differed significantly between PE and controls and was particularly significant in severe PE subgroup and early-onset PE subgroup. PTPRK is primarily localized in placental trophoblast cells. The mRNA and protein levels of PTPRK in PE were significantly higher than those in controls.
Conclusion:
These results suggest that PTPRK appears to be a previously unrecognized susceptibility gene for PE in Han Chinese women, and its expression is also associated with PE, while ROS1 rs9489124 has no apparent correlation with PE risk.
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