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Circulating fragmented mitochondria induce maternal hypertension, placental inflammation and apoptosis in pregnant rats

Mitochondrial fragments released from necrotic cells (mitochondrial damage‐associated molecular patterns, mitDAMPs) have pro‐inflammatory and immunogenic properties. Placentas from pregnancies with preeclampsia (PE) show exaggerated rates of cell death. We tested the hypothesis that circulating fragmented mitochondria would increase maternal blood pressure and induce placental inflammation and apoptosis in pregnant rats. Mitochondria were isolated from rat liver and sonication was used to disrupt their integrity. Pregnant rats were injected with fragmented mitochondria (mit‐treated; 4 mg/tissue) or saline (control) on gestational day (gd) 15. On gd17, systolic blood pressure, as measured with the tail cuff method, was increased in mit‐treated compared to saline‐treated dams (mit‐treated vs. control: 140±3 vs. 114±6 mmHg, p<0.05). Protein levels of cyclooxygenase 1 (COX1) and 2 (COX2) and pro‐apoptotic protein BAX were increased in placentas from mit‐treated rats (mit‐treated vs. control: COX1, 6.3±1.8 vs. 1.9±1.3; COX2, 2.6±0.2 vs. 1.7±0.3; BAX: 9.1±1.3 vs. 4.4±0.02, p<0.05). Systemic treatment with fragmented mitochondria increases maternal blood pressure, placental inflammation and apoptosis in pregnant rats. MitDAMPs released from necrotic trophoblasts may be the source of maternal hypertension and placental dysfunction in pregnancies with PE.