[200-POS]: Inflammatory gene expressions of adipose tissue under preeclamptic culture condition

Increased insulin resistance in preeclampsia has been regarded as a key mechanism for the establishment of the disease. Additionally, inflammatory action including adipocytokine production and homeostatic inflammation is shown as a critical pathway of pathophysiology of preeclampsia. To investigate the inflammatory pathway within tissue, we established new culture system of adipose tissue on the bottom of the plate ("gel-bottom capture") with preeclampsia serum, and quantified the expressions of inflammation-related genes using paneled-array method.Visceral fat (omentum) was obtained from the patients at reproductive age that had omentectomy with gynecological reason, which confirmed no metastasis of cancer. Tissue was captured on the bottom of culture plate using Peptide Hydrogel (BD Biosciences, Inc.) and incubated at 37°C for 24h with 10% serum from five severe preeclampsia or five gestational age-matched normotensive women. After extractions of total mRNA, 370 genes set related to inflammation were analyzed with inflammation-targeted PCR array (RT(2) Profiler™ PCR Array, Qiagen Inc.).The viability of the tissue was not altered after 24h culture. 30 genes related inflammation in the adipose tissue showed statistically significant increase or decrease in preeclamptic culture compared to normal pregnancy. Altered genes were related to chemokine, inflammatory action including toll-like receptor and ligands, insulin resistance and adipogenesis, which plays a central role in systemic inflammation of preeclampsia. However, beneficial genes in regulation of Th2 predominance, anti-oxidative stress and insulin sensitivity were also defined.Under our newly innovated culture method, it was firstly revealed that adipose tissue effects on both systemic inflammation and protection against inflammation or oxidative stress under preeclamptic serum. It suggested that the adipose tissue acts as a key organ of the pathogenesis of preeclampsia.J. Akasaka: None. K. Naruse: None. N. Koike: None. A. Shigemitsu: None. K. Iwai: None. H. Kobayashi: None.