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High mobility group box 1 (HMGB1) levels in the placenta and in serum in preeclampsia
Authors:Wang Bo  Koga Kaori  Osuga Yutaka  Hirata Tetsuya  Saito Ako  Yoshino Osamu  Hirota Yasushi  Harada Miyuki  Takemura Yuri  Fujii Tomoyuki  Taketani Yuji
Affiliation:Department of Obstetrics and Gynecology, University of Tokyo, 7-3-1 Hongo, Tokyo, Japan.
Abstract:Citation
Wang B, Koga K, Osuga Y, Hirata T, Saito A, Yoshino O, Hirota Y, Harada M, Takemura Y, Fujii T, Taketani Y. High mobility group Box 1 (HMGB1) levels in the placenta and in serum in preeclampsia. Am J Reprod Immunol 2011; 66: 143–148 Problem Preeclampsia is a pregnancy disorder characterized by systemic inflammation. High mobility group box 1 (HMGB1) is a molecule known to act as a ‘danger signal’ by participating in various inflammatory processes, but data in regard to preeclampsia are sparse. The aim of this study was to analyze placental and serum HMGB1 levels in normal pregnancy and preeclampsia. Method of study Sera were collected from women with preeclampsia soon after the manifestation of the disease and before commencing any medication. Placental samples were collected immediately after delivery. Expressed isoforms of HMGB1 (28‐ and 30‐kDa) in the placenta were evaluated by Western blot analysis. Serum HMGB1 concentrations were measured using enzyme‐linked immunosorbent assays (ELISA). Results Two isoforms of HMGB1 are expressed by the human placenta. The 28‐ and 30‐kDa HMGB1 isoforms were expressed highly in preeclamptic placental tissue; however, compared with normotensive control tissue, differences in detected expression levels did not reach statistical significance. No significant difference was observed in serum HMGB1 levels between control and preeclampsia. Conclusion Inflammation provoked by HMGB1 is likely to be involved in the proinflammatory process in preeclamptic placenta. Further studies are needed to elucidate the precise role of HMGB1 in preeclampsia.
Keywords:Apoptosis  hypoxia  inflammation  oxidative stress  receptor for advanced glycation end products  toll‐like receptors
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