19: Effect of sFLT-1 over-expression on blodd pressure of mice in their second pregnancy

Article Outline

• Objective
• Study design
• Results
• Conclusion
• Copyright

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Objective 

sFlt-1 is believed to play a role in the pathogenesis of preeclampsia. Over-expression of sFlt-1 in pregnant mice produces a preeclampsia-like condition. Given that the rate of preeclampsia in nulliparous women is higher than in women who have had a prior pregnancy, we hypothesized that over-expresion of sFlt-1 in mice in their second pregnancy would not result in the preeclampsia-like condition as in the first. Our aim in this study was to evaluate the effect of sFlt-1 over-expression on blood pressure (BP) using mice in their subsequent pregnancy.

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Study design 

CD-1 mice at day 8 of gestation were injected with the adenovirus carrying sFlt-1 (10⁹ PFU; sFlt-1 group) or the murine IgG2 α Fc fragment (10⁹ PFU; mFc group as the virus control). At day 11 of gestation, BP catheters were inserted into the aortic arch and tunneled to a telemetric transmitter. BP was monitor continuously in the conscious unrestrained animals until day 18 of pregnancy, at this time mice were sacrificed, blood was collected and placentas/fetuses were counted and weighted. Student t test was used for statistical analysis (significance: p<0.05).

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Results 

Our previous data showed that over-expression of sFlt-1 in mice in their first pregnancy leads to increase in mean BP, fetal growth restriction, low platelet, and higher hematocrit. However, when mice in their second pregnancy were evaluated, mean BP, average pups/placental weight, as well all the maternal hematological parameters (platelet, white cell count, hemoglobin, hematocrit, serum creatinine, uric acid) did not differ between the sFlt-1 and mFc groups.

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Conclusion 

Our results confirm the similarity between the sFlt-1 animal model and preeclampsia in humans. A prior pregnancy appears to confer a protective mechanism against the effect of inhibition of angiogenic factors by sFlt-1. Further evaluation of these mechanisms may improve our knowledge of the pathogenesis of preeclampsia, and provide novel avenues for prevention.