Abstract
Objectives. The pathophysiology of preeclampsia is characterized by abnormal placentation, an exaggerated inflammatory response, and generalized dysfunction of the maternal endothelium. We investigated the effects of preeclampsia serum on the expression of inflammation-related genes by adipose tissue. Materials and Methods. Visceral adipose tissue was obtained from the omentum of patients with early ovarian cancer without metastasis. Adipose tissue was incubated with sera obtained from either five women affected with severe preeclampsia or five women from control pregnant women at 37°C in a humidified incubator at 5% CO2 for 24 hours. 370 genes in total mRNA were analyzed with quantitative RT-PCR (Inflammatory Response & Autoimmunity gene set). Results. Gene expression analysis revealed changes in the expression levels of 30 genes in adipose tissue treated with preeclampsia sera. Some genes are related to immune response, oxidative stress, insulin resistance, and adipogenesis, which plays a central role in excessive systemic inflammatory response of preeclampsia. In contrast, other genes have shown beneficial effects in the regulation of Th2 predominance, antioxidative stress, and insulin sensitivity. Conclusion. In conclusion, visceral adipose tissue offers protection against inflammation, oxidative insults, and other forms of cellular stress that are central to the pathogenesis of preeclampsia.
Highlights
Preeclampsia is the leading cause of pregnancy-associated maternal and perinatal mortality and morbidity worldwide
A normal pregnancy enhances a state of the T helper 2 (Th2) type anti-inflammatory responses, preeclampsia exhibits a shift towards Th1 [4, 7] and Th17 [8] type immunity
Thirty genes were identified with altered expression of at least 2-fold or statistical significance (P < 0.05, unpaired t test) in adipose tissues treated with preeclampsia sera (Figure 1, Table 2)
Summary
Preeclampsia is the leading cause of pregnancy-associated maternal and perinatal mortality and morbidity worldwide. This disorder affects approximately 5% of all pregnancies. Several mechanisms have been proposed in preeclampsia, including (1) genetics and epigenetic imprinting; (2) increased uteroplacental ischemia/hypoxia; (3) angiogenic imbalances characterized by an excess of antiangiogenic factors; (4) increased trophoblast apoptosis/necrosis; (5) an exaggerated maternal inflammatory response to injured trophoblast cells; and (6) immune maladaptation [1]. Placenta-derived circulating factors could stimulate proinflammatory cells to produce cytokines and chemokines, including IL-1beta, IL-2, IL-10, IL-12, IL-13, IL-18, granulocyte-colony stimulating factor (G-CSF), interferon- (IFN-) gamma, monocyte chemoattractant protein-1 (MCP-1), and TNF-alpha, demonstrating that preeclampsia is associated with an overall proinflammatory systemic environment [4–6]. A normal pregnancy enhances a state of the T helper 2 (Th2) type anti-inflammatory responses, preeclampsia exhibits a shift towards Th1 [4, 7] and Th17 [8] type immunity
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