Inflammatory Mediators Associated with Pre-eclampsia
PURPOSE: Pre-eclampsia, a hypertensive disorder unique in pregnancy, complicates approximately 5-7 % of pregnancies and is a leading cause of intrauterine fetal growth retardation, premature delivery, and maternal death. It is characterized by proteinuria, edema, platelet aggregation, and increased vasoconstriction leading to maternal hypertension and uteroplacental blood flow reduction. Macrophages normally play a key role in implantation, placenta formation and parturition. Indeed, macrophages are one of the major cell types in both the maternal and fetal compartments of the uteroplacental unit. Oxidized lipids in the maternal circulation might cause inflammation of the endothelium leading to expression of cytokines. It has been suggested that the increased level of inflammatory cytokines might be related to pre-eclampsia. Therefore, the purpose of this research was to prove the relationship between the inflammatory molecules and pre-eclampsia. MATERIALS AND METHODS: The presence of macrophages in placental tissues was analyzed by FACS after staining cells with a-CD68 antibody. Inflammation mediated molecules (NF-kB, p-JNK, iNOS, COX-2) were analyzed by Western blotting and RT-PCR. RESULTS AND CONCLUSION: First, Significant levels of macrophages were detected in both normal and patient groups. Second, Western blotting was also performed to analyze protein levels of NF-kB, p-JNK and iNOS in the placental decidual tissue of both groups. Samples from preeclampsia patients had higher levels of NF-kB, p-JNK and iNOS than normal group. In addition, analysis of mRNA levels showed that although Patient group had higher NF-kB, iNOS, COX-2 mRNA levels than normal group, there was no difference in JNK1 mRNA levels between them. The results from the experiments suggest that macrophages are not only increase in numbers but also are activated to increase level of inflammatory mediators, NF-kB, JNK, iNOS and COX-2, and this phenomena may be related to pre-eclampsia. These results may provide new insights into the key mechanisms that trigger pre-eclampsia and new therapeutic targets that will improve the management of Pre-eclampsia.
전자간증, 대식세포, 탈락막, 태반, CD68, NF-kB, JNK, iNOS, COX-2, 염증, Pre-eclampsia, macrophage, decidual, placenta, inflammation
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