TY - JOUR
T1 - Alpha 1 antitrypsin activity is decreased in human amnion in premature rupture of the fetal membranes
AU - Izumi-Yoneda, Noriko
AU - Toda, Ayaka
AU - Okabe, Motonori
AU - Koike, Chika
AU - Takashima, Seiji
AU - Yoshida, Toshiko
AU - Konishi, Ikuo
AU - Saito, Shigeru
AU - Nikaido, Toshio
N1 - Funding Information:
This work was supported in part by Grants-in-Aid 16390473, 16650102 and 20390430 for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, Japan.
PY - 2009
Y1 - 2009
N2 - 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.
AB - 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.
KW - Alpha 1 antitrypsin
KW - Amnion
KW - MMP9
KW - Oxidization
KW - PPROM
UR - http://www.scopus.com/inward/record.url?scp=60149100930&partnerID=8YFLogxK
U2 - 10.1093/molehr/gan071
DO - 10.1093/molehr/gan071
M3 - 学術論文
C2 - 19073710
AN - SCOPUS:60149100930
SN - 1360-9947
VL - 15
SP - 49
EP - 57
JO - Molecular Human Reproduction
JF - Molecular Human Reproduction
IS - 1
ER -