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Postpartum increases in cerebral edema and inflammation in response to placental ischemia during pregnancy

Ahsia M. Clayton, Qingmei Shao, Nina D. Paauw, Ashtin B. Giambrone, Joey P. Granger, Junie P. Warrington

Brain Behav Immun. 2018, 70:376-389.

DOI:10.1016/j.bbi.2018.03.028

https://www.sciencedirect.com/science/article/pii/S0889159118300813?via%3Dihub

June Paula Warrington (USA)


1)      Summarize your work in one sentence.

The aim of this study was to determine whether reduced blood flow to the developing placenta and fetus, as occurs in preeclampsia, contributes to postpartum brain abnormalities such as inflammation and edema in a rat preclinical model.


2) Summarize your findings in one sentence.

Two months after delivery, rats subjected to reduced placental blood flow (placental ischemia) during pregnancy had evidence of brain edema and tissue inflammation measured as increased neuroglial cell activation, increased pro-inflammatory cytokines, and reduced blood-brain barrier associated protein, occludin.


2)      Which were the more important methods you used in this work? If it is not a traditional method you can briefly explain the concept of that methodology.

We reduced the size of the blood vessels that supply the placenta and fetus in pregnant rats by surgically placing silver clips of specified diameters, causing placental ischemia. Dams were allowed to deliver and 2 months later, brains were collected, dissected, and processed for fluorescence staining or protein extraction. Molecular assays were used to measure concentrations of 27 cytokines/chemokines, and using immunofluorescence staining, astrocyte and microglia activation was assessed.


3)      What did you learn from this paper, what was your take-home message?

The rat model of placental ischemia can be used as a tool to assess mechanisms underlying long-term cerebrovascular abnormalities reported in women with a history of preeclampsia. Findings from this study also support the hypothesis that neuroinflammation may be an underlying factor mediating long-term cerebrovascular complications following preeclampsia.

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