MMP-15 is localised to the syncytiotrophoblast and up-regulated in preeclamptic placenta.

<p>Representative immunohistochemistry for endoglin (<b>A, B</b>) and MMP-15 (<b>D, E</b>), shows both proteins localize to the syncytiotrophoblast in pre-eclamptic (<b>A, D</b>) and pre-term control (<b>B, E</b>) placentas. Immunohistochemistry on serial sections (2 µm) of placenta revealed co-localisation of endoglin (<b>G</b>) and MMP-15 (<b>H</b>) to the syncytiotrophoblast. No staining was observed in isotype controls (<b>C, F</b>). Densitometric analysis of western blots for MMP-15 (<b>I, J</b>) revealed a significant increase in preeclamptic placentas (n = 8) compared to pre-term controls (n = 8). *p≤0.05.</p

MMP-15 inhibtion does not decrease soluble endoglin production <i>in vitro</i>.

<p>Treatment of HUVEC cells (<b>A)</b> and syncytialised BeWo cells (<b>B</b>) with MMP-14 siRNA alone or in combination with MMP-15 siRNA induced a significant decline in sEng production compared to scrambled siRNA, whilst MMP-15 siRNA alone had no effect. Data shown as mean±SEM, n = 3 experiments, *p≤0.05.</p

Clinical Characteristics of the preeclamptic cohort.

<p>Shown are clinical details of the two cohorts from whom we obtained placentas for our analyses. The preeclamptic cohort all had severe preeclampsia necessitating delivery preterm. Preterm controls where those who were delivered early for other indications but did not have preeclampsia. **p<0.001. SEM =  standard error of the mean, SBP =  systolic blood pressure, DBP =  diastolic blood pressure, BMI =  body mass index and GA =  gestational age.</p