Tamara Antonic, Sandra Vladimirov, Daniela Ardalic, Milica Miljkovic-Trailovic, Marija Saric-Matutinovic, Tamara Gojkovic, Jelena Munjas, Jasmina Ivanisevic, Snezana Jovicic, Jelena Vekic, Aleksandra Zeljkovic, Zeljko Mikovic, Aleksandra Stefanović
{"title":"揭示迟发型子痫前期鞘脂动力学:来自脂质组学分析的见解。","authors":"Tamara Antonic, Sandra Vladimirov, Daniela Ardalic, Milica Miljkovic-Trailovic, Marija Saric-Matutinovic, Tamara Gojkovic, Jelena Munjas, Jasmina Ivanisevic, Snezana Jovicic, Jelena Vekic, Aleksandra Zeljkovic, Zeljko Mikovic, Aleksandra Stefanović","doi":"10.11613/BM.2025.010708","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Sphingolipids, essential to trophoblast and endothelial function, may impact inflammation in preeclampsia. However, their specific role in late-onset preeclampsia remains unclear. To address this research gap, we analyzed sphingolipid profiles in pregnancies at high risk for preeclampsia development to identify potential biomarkers and clarify their role in disease pathogenesis.</p><p><strong>Materials and methods: </strong>We monitored 90 pregnant women at high risk for preeclampsia development across four gestational points. These women were later categorized into the group of women with high risk who did not develop preeclampsia (HRG) (70 women) or the preeclampsia group (PG) (20 women). Sphingolipids (sphingosine, sphinganine, sphingosine-1-phosphate (S1P), ceramides C16:0/C24:0, and sphingomyelin C16:0) were quantified via liquid chromatography-tandem mass spectrometry.</p><p><strong>Results: </strong>Sphingolipid profiles revealed distinct patterns between groups. Concentrations of S1P in the HRG increased from the 1st trimester to delivery (P < 0.001). We did not notice significant changes in S1P during pregnancy in the PG but compared with the HRG we found significantly lower concentrations at each test point from the 2nd trimester until delivery (P = 0.020, P = 0.013, P = 0.011, respectively). Ceramides C16:0 and C24:0 demonstrated significant increases over time in HRG (P < 0.001, both). Sphingomyelin C16:0 increased significantly across pregnancy in both groups (P < 0.001 in HRG and P = 0.006 in PG), with no significant differences between groups.</p><p><strong>Conclusions: </strong>We identified S1P as a potential biomarker for late-onset preeclampsia, with lower concentrations observed in PG compared to HRG. Rising sphingomyelin concentrations in both cohorts might serve as a relevant cardiovascular risk indicator in pregnancies at high risk for preeclampsia.</p>","PeriodicalId":94370,"journal":{"name":"Biochemia medica","volume":"35 1","pages":"010707"},"PeriodicalIF":0.0000,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11838718/pdf/","citationCount":"0","resultStr":"{\"title\":\"Unraveling sphingolipid dynamics in late-onset preeclampsia: insights from lipidomic analysis.\",\"authors\":\"Tamara Antonic, Sandra Vladimirov, Daniela Ardalic, Milica Miljkovic-Trailovic, Marija Saric-Matutinovic, Tamara Gojkovic, Jelena Munjas, Jasmina Ivanisevic, Snezana Jovicic, Jelena Vekic, Aleksandra Zeljkovic, Zeljko Mikovic, Aleksandra Stefanović\",\"doi\":\"10.11613/BM.2025.010708\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Sphingolipids, essential to trophoblast and endothelial function, may impact inflammation in preeclampsia. However, their specific role in late-onset preeclampsia remains unclear. To address this research gap, we analyzed sphingolipid profiles in pregnancies at high risk for preeclampsia development to identify potential biomarkers and clarify their role in disease pathogenesis.</p><p><strong>Materials and methods: </strong>We monitored 90 pregnant women at high risk for preeclampsia development across four gestational points. These women were later categorized into the group of women with high risk who did not develop preeclampsia (HRG) (70 women) or the preeclampsia group (PG) (20 women). Sphingolipids (sphingosine, sphinganine, sphingosine-1-phosphate (S1P), ceramides C16:0/C24:0, and sphingomyelin C16:0) were quantified via liquid chromatography-tandem mass spectrometry.</p><p><strong>Results: </strong>Sphingolipid profiles revealed distinct patterns between groups. Concentrations of S1P in the HRG increased from the 1st trimester to delivery (P < 0.001). We did not notice significant changes in S1P during pregnancy in the PG but compared with the HRG we found significantly lower concentrations at each test point from the 2nd trimester until delivery (P = 0.020, P = 0.013, P = 0.011, respectively). Ceramides C16:0 and C24:0 demonstrated significant increases over time in HRG (P < 0.001, both). Sphingomyelin C16:0 increased significantly across pregnancy in both groups (P < 0.001 in HRG and P = 0.006 in PG), with no significant differences between groups.</p><p><strong>Conclusions: </strong>We identified S1P as a potential biomarker for late-onset preeclampsia, with lower concentrations observed in PG compared to HRG. 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引用次数: 0
摘要
神经鞘脂对滋养细胞和内皮功能至关重要,可能影响子痫前期的炎症。然而,它们在迟发性先兆子痫中的具体作用尚不清楚。为了弥补这一研究空白,我们分析了子痫前期高风险孕妇的鞘脂谱,以确定潜在的生物标志物并阐明其在疾病发病机制中的作用。材料和方法:我们在四个妊娠期监测了90名高危子痫前期孕妇。这些妇女随后被分为未发生子痫前期的高风险妇女组(HRG)(70名妇女)和子痫前期妇女组(PG)(20名妇女)。采用液相色谱-串联质谱法定量测定鞘磷脂(鞘磷脂、鞘氨酸、鞘磷脂-1-磷酸(S1P)、神经酰胺C16:0/C24:0和鞘磷脂C16:0)。结果:鞘脂谱在各组间显示出不同的模式。HRG中S1P的浓度从妊娠早期到分娩增加(P < 0.001)。我们没有注意到妊娠期间PG中S1P的显著变化,但与HRG相比,我们发现从妊娠中期到分娩的每个测试点S1P的浓度都显著降低(P = 0.020, P = 0.013, P = 0.011)。神经酰胺C16:0和C24:0随着时间的推移在HRG中表现出显著的增加(P均< 0.001)。两组Sphingomyelin C16:0在妊娠期间均显著升高(HRG组P < 0.001, PG组P = 0.006),组间差异无统计学意义。结论:我们确定S1P是迟发性子痫前期的潜在生物标志物,与HRG相比,PG中的S1P浓度较低。两个队列中鞘磷脂浓度升高可能是子痫前期高危妊娠的相关心血管风险指标。
Unraveling sphingolipid dynamics in late-onset preeclampsia: insights from lipidomic analysis.
Introduction: Sphingolipids, essential to trophoblast and endothelial function, may impact inflammation in preeclampsia. However, their specific role in late-onset preeclampsia remains unclear. To address this research gap, we analyzed sphingolipid profiles in pregnancies at high risk for preeclampsia development to identify potential biomarkers and clarify their role in disease pathogenesis.
Materials and methods: We monitored 90 pregnant women at high risk for preeclampsia development across four gestational points. These women were later categorized into the group of women with high risk who did not develop preeclampsia (HRG) (70 women) or the preeclampsia group (PG) (20 women). Sphingolipids (sphingosine, sphinganine, sphingosine-1-phosphate (S1P), ceramides C16:0/C24:0, and sphingomyelin C16:0) were quantified via liquid chromatography-tandem mass spectrometry.
Results: Sphingolipid profiles revealed distinct patterns between groups. Concentrations of S1P in the HRG increased from the 1st trimester to delivery (P < 0.001). We did not notice significant changes in S1P during pregnancy in the PG but compared with the HRG we found significantly lower concentrations at each test point from the 2nd trimester until delivery (P = 0.020, P = 0.013, P = 0.011, respectively). Ceramides C16:0 and C24:0 demonstrated significant increases over time in HRG (P < 0.001, both). Sphingomyelin C16:0 increased significantly across pregnancy in both groups (P < 0.001 in HRG and P = 0.006 in PG), with no significant differences between groups.
Conclusions: We identified S1P as a potential biomarker for late-onset preeclampsia, with lower concentrations observed in PG compared to HRG. Rising sphingomyelin concentrations in both cohorts might serve as a relevant cardiovascular risk indicator in pregnancies at high risk for preeclampsia.