Proteomics Analysis Reveals Abnormal Electron Transport and Excessive Oxidative Stress Cause Mitochondrial Dysfunction in Placental Tissues of Early-Onset Preeclampsia.

PurposeEarly-onset preeclampsia (EOS-PE) refers to preeclampsia that occurred before 34 gestation weeks. This study is conducted to explore the relationship between mitochondrial dysfunction and the pathogenesis of EOS-PE using proteomic strategy. Experimental designTo identify altering expressed mitochondrial proteins between severe EOS-PE and healthy pregnancies, enrichment of mitochondria coupled with iTRAQ-based quantitative proteomic method is performed. Immunohistochemistry (IHC) and western blot are performed to detect the alteration of changing expression proteins, and confirmed the accuracy of proteomic results. ResultsA total of 1372 proteins were quantified and 132 altering expressed proteins were screened, including 86 downregulated expression proteins and 46 upregulated expression proteins (p<0.05). Bioinformatics analysis showed that differentially expressed proteins participated in numerous biological processes, including oxidation-reduction process, respiratory electron transport chain, and oxidative phosphorylation. Especially, mitochondria-related molecules, PRDX2, PARK7, BNIP3, BCL2, PDHA1, SUCLG1, ACADM, and NDUFV1, are involved in energy-production process in the matrix and membrane of mitochondria. Conclusions and clinical relevanceResults of the experiment show that abnormal electron transport, excessive oxidative stress, and mitochondrion disassembly might be the main cause of mitochondrial dysfunction, and is related to the pathogenesis of EOS-PE.