Preeclampsia (PE) is one of the most common obstetrical complications, affecting ~5-7% of all pregnancies worldwide. Hallmarked by new-onset hypertension, maternal vascular dysfunction, and end organ injury, PE can potentially progress to eclampsia; a condition that results in grand mal seizures, and risks mortality. While the origins of the disease are not entirely clear, it is now well-established that placental insufficiency is a central component of most preeclampsia cases. In response to chronic ischemia, the innate immune response becomes involved, and inflammatory cytokines are released locally within the placenta and hence into the maternal circulation. While this response is known, and a number of immune cell types have been implicated, little work has examined the role of resident mast cells in the placental response to hypoxia. We hypothesized that resident placental mast cells would release inflammatory cytokines in response to hypoxia and serum from rats with placental ischemia, and would release factors that would inhibit endothelial and placental trophoblast function. In response to serum from rodents with placental ischemia, cultured mast cells exhibited increased mRNA expression of TNF-α (100±5 vs 265±13%, p< 0.05) and IL-6 (100±9 vs 387±36%, p< 0.05) when compared to control pregnant rodent serum. Furthermore, hypoxia simulating PE placentas (1% oxygen) caused a significant increase in TNF-α (100±2 vs 525±21%, p< 0.05) and IL6 (100±5 vs 458±38%, p< 0.05) mRNA expression when compared to control oxygen. Finally, we found that conditioned media from cultured mast cells exposed to hypoxia for 24 hours significantly inhibited endothelial cell proliferation by MTS assay. Taken together, these data suggest that hypoxia causes resident placental mast cells to increase inflammatory cytokine production, release factors that inhibit endothelial cell proliferation, and that factors in PE rodents activate mast cells. Future studies will examine the in vivo effects of mast cell activation and inhibition in a PE model. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Pruett et al. (Fri,) studied this question.