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Mol. Hum. Reprod. Advance Access originally published online on December 10, 2008
Molecular Human Reproduction 2009 15(1):49-57; doi:10.1093/molehr/gan071
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© The Author 2008. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Alpha 1 antitrypsin activity is decreased in human amnion in premature rupture of the fetal membranes

Noriko Izumi-Yoneda1,2, Ayaka Toda1, Motonori Okabe1, Chika Koike1, Seiji Takashima3, Toshiko Yoshida1, Ikuo Konishi4, Shigeru Saito2 and Toshio Nikaido1,5

1Department of Regenerative Medicine, University of Toyama Graduate School of Medicine and Pharmaceutical Sciences, Toyama, Japan 2Department of Obstetrics and Gynecology, University of Toyama Graduate School of Medicine and Pharmaceutical Sciences, Toyama, Japan 3Department of Biomolecular Engineering, Tokyo Institute of Technology, Tokyo, Japan 4Department of Obstetrics and Gynecology, Kyoto University Graduate School of Medicine, Kyoto, Japan

5 Correspondence address. Tel: +81-76-434-7210; Fax: +81-76-434-5011; E-mail: tnikaido{at}med.u-toyama.ac.jp

Preterm premature rupture of the membranes (PPROM) has been considered to be closely associated with chorioamnionitis. However, the detailed mechanism is not well understood. Alpha 1 antitrypsin (AAT) was reported to decrease in concentration in amniotic fluid obtained from patients with PPROM. However, the origin of AAT in amniotic fluid has not been clarified. In this study, we assessed the expression and localization of AAT in human amnion, as well as its biological activity in cases with PROM. Human amniotic epithelial (hAE) cells expressed AAT. After stimulation with oncostatin M (OSM), interleukin-6 (IL-6) or tumor necrotic factor alpha (TNF {alpha}), hAE cells increased the expression of AAT, while the expression of MMP9 was reduced by OSM and induced by TNF {alpha}. Oxidized AAT (inactivated form) was detected in the amnion with PPROM and TPROM, but not in specimens without PROM. Moreover, AAT activity was decreased in amnions from cases with PROM, regardless of gestational age. Thus, the results showed that AAT in the amnion may function as a protective shield at inflammatory sites, and not as it loses it inhibitory activity in cases with PROM, possibly by oxidation, suggesting that its imbalance contributes to PROM.

Key words: amnion/alpha 1 antitrypsin/oxidization/MMP9/PPROM

Submitted on October 24, 2007; resubmitted on November 14, 2008; accepted on November 18, 2008.


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