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

Noriko Izumi-Yoneda, Ayaka Toda, Motonori Okabe, Chika Koike, Seiji Takashima, Toshiko Yoshida, Ikuo Konishi, Shigeru Saito, Toshio Nikaido*

*この論文の責任著者

研究成果: ジャーナルへの寄稿学術論文査読

23 被引用数 (Scopus)

抄録

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 α), hAE cells increased the expression of AAT, while the expression of MMP9 was reduced by OSM and induced by TNF α. 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.

本文言語英語
ページ(範囲)49-57
ページ数9
ジャーナルMolecular Human Reproduction
15
1
DOI
出版ステータス出版済み - 2009

ASJC Scopus 主題領域

  • 医学一般

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