Preeclampsia is characterized by new onset hypertension and proteinuria after 20 weeks gestation. Though the pathophysiology has not been fully defined, preeclampsia is thought to begin when the fetal trophoblastic cells and maternal endothelial cells fail to adequately remodel to supply blood to the fetus. This placental ischemia results in the release of maternal factors such as cytokines – those studied in this paper are adiponectin and leptin. Both of these are released by white adipose tissue and, during pregnancy, are involved in trophoblastic invasion. These cytokines are mediated by metalloproteinases (MMPs) such as MMP2 and MMP9 and their inhibitors (TIMP1 and TIMP2).
In this study, adiponectin, leptin, MMP2, MMP9, TIMP1, and TIMP2 plasma concentrations were compared between healthy pregnancies and preeclamptic pregnant groups. ELISA kits were used to measure the concentrations and Student’s t-test, the chi-squared test, and the Pearson’s correlation test were performed on the data. Maternal age, BMI, MMP9 levels, MMP9/TIMP1 and MMP2/TIMP2 ratios were not statistically different from each other. Both systolic and diastolic blood pressure were higher, and gestational age at sampling, delivery, and newborn weight were lower in the preeclamptic group compared to the HP group. Leptin, adiponectin, TIMP1, TIMP2, and MMP2 were higher in the preeclamptic group as well.
I think the paper is relevant and the experimental approach is sound. The significance point for the data is P<0.05, which is not different from many other papers published in various journals. The paper’s authors say comment that, to their knowledge, “This is the first study to measure correlation between circulating adiponectin and leptin and MMP/TIMP concentrations in preeclamptic patients, even though both have been shown to be related to trophoblast invasion” (Eleuterio, et al. 2015). The results show that the study is relevant and matches the stated objective of the paper in the abstract. All the cytokines and metalloproteinases measured were higher in preeclamptic patients, showing that, clearly, the study was needed.
Future studies could either block the production or interfere with the activity of adiponectin, leptin, or the metalloproteinases in animal models of preeclampsia or in endothelial cell cultures. These studies could monitor the effects on the other cytokines and proteinases or on the symptoms such as placental ischemia. The authors also suggested that adiponectin may contribute to higher levels of MMP2 and TIMP2, so studies could be done to elucidate that relationship.
Eleuterio, Nibia Mariana, et al. “Positive Correlations Between Circulating Adiponectin and MMP2 in Preeclampsia Pregnant.” Pregnancy Hypertension: An International Journal of Women’s Cardiovascular Health 5. (2015): 205-208. ScienceDirect. Web. 9 Sept. 2016.