Progesterone‐induced blocking factor blockade causes hypertension in pregnant rats

Preeclampsia (PE) is a multisystem disorder characterized by new onset hypertension in mid‐late gestation and can include multi‐organ dysfunction with or without proteinuria. It affects 5%–7% of all pregnancies in the U.S., making PE a major contributor to maternal and fetal morbidity and mortality....

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Bibliographic Details
Published in:American journal of reproductive immunology (1989) 2024-01, Vol.91 (1), p.e13805-n/a
Main Authors: Meadors, Alexis, Comley, Kyleigh, Cottrell, Jesse N., Ibhahim, Tarek, Cunningham, Mark W., Amaral, Lorena M.
Format: Article
Language:English
Subjects:
Blood pressure
Fetuses
Gestation
Helper cells
Hypertension
Hypotheses
Immunoglobulin G
Inflammation
Lymphocytes T
Morbidity
Natural killer cells
Pre-eclampsia
Preeclampsia
Pregnancy
Pregnancy complications
Progesterone
progesterone‐induced blocking factor
Proteinuria
Renal cortex
Signal transduction
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Summary:Preeclampsia (PE) is a multisystem disorder characterized by new onset hypertension in mid‐late gestation and can include multi‐organ dysfunction with or without proteinuria. It affects 5%–7% of all pregnancies in the U.S., making PE a major contributor to maternal and fetal morbidity and mortality. Currently, there is no cure for this pregnancy complication except for early delivery of the placenta and fetus. Moreover, the therapeutic options to treat PE are very limited. One potential trigger for the development of PE is progesterone deficiency‐induced imbalance between T Helper 1(Th1)/Th2 cells, an increase in cytolytic natural killer (NK) cells and inflammatory cytokines that in turn leads to endothelial dysfunction, intrauterine growth restriction (IUGR) and hypertension. Importantly, progesterone signals the synthesis of progesterone‐induced blocking factor (PIBF) which has anti‐inflammatory effects and could promote the regulation of inflammation balance during pregnancy. However, the role of progesterone and PIBF in the pathophysiology of PE is still not fully understood. Thus, this current study was designed to test the hypothesis that inhibition of PIBF causes signs of PE in pregnant Sprague Dawley rats. In order to address our hypothesis, rabbit anti‐PIBF IgG (0.25, low dose‐LD or 0.50 mg/mL, high dose‐HD) was administered intraperitoneally on gestation day (GD) 15 to normal pregnant Sprague Dawley (NP) rats. On GD 18, carotid catheters were inserted and on GD 19 mean blood pressure (MAP) and samples were collected for further analysis. MAP in normal pregnant rats (NP) rats (n = 7) was 99 ± 3 mmHg, which increased to 116 ± 2 mmHg in NP+ anti‐PIBF LD (n = 10) and 113 ± 4 mmHg in NP+ anti‐PIBF HD (n = 4), p 
ISSN:1046-7408
1600-0897
DOI:10.1111/aji.13805