Fetal membranes as an interface between inflammation and metabolism: increased aquaporin 9 expression in the presence of spontaneous labor at term and chorioamnionitis.
OBJECTIVE
Aquaporin 9 (AQP9) is a water channel protein characterized by its high permeability to nutrients such as lactate and glycerol, as well as urea and other small solutes. These unique properties of AQP9 suggest that this molecule may play a role in the modulation of nutrient flux through the fetal membranes in conditions associated with increased metabolic demand, such as spontaneous labor and inflammation. The objective of this study was to determine the expression of AQP9 in the chorioamniotic membranes from women with and without term labor, as well as those with preterm prelabor rupture of membranes (PPROM) with and without histologic chorioamnionitis.


METHODS
A cross-sectional study was performed which included patients in the following groups: (1) term not in labor (TNL; n = 14); (2) term, spontaneous labor (n = 14); and (3) PPROM with (n = 20) and without (n = 17) histologic chorioamnionitis. AQP9 mRNA expression in fetal membranes was quantified using quantitative real-time reverse transcription-polymerase chain reaction and analyzed with a linear model including gestational age as a covariate.


RESULTS
(1) AQP9 mRNA expression was identified in all chorioamniotic membrane specimens; (2) AQP9 expression in fetal membranes was significantly higher in spontaneous term labor when compared with TNL (fold change 3.6; p = 0.01); and (3) Among patients with PPROM, the presence of histologic chorioamnionitis was associated with a higher expression of AQP9 in the chorioamniotic membranes compared with those from women without histologic chorioamnionitis (fold change 8.7; p < 0.001).


CONCLUSIONS
Aquaporin 9 mRNA expression is higher in the fetal membranes from patients with spontaneous term labor and those with PPROM and histologic chorioamnionitis. These findings are novel, and suggest a role for aquaporin 9 in membrane-mediated transfer of nutrients to support the increased metabolic demands associated with the host immune response of the terminal pathway of parturition and histologic chorioamnionitis.
Mittal
Pooja
P
Perinatology Research Branch, NICHD, NIH, DHHS, Detroit, Michigan, USA.
Romero
Roberto
R
Mazaki-Tovi
Shali
S
Tromp
Gerard
G
Tarca
Adi L
AL
Kim
Yeon Mee
YM
Chaiworapongsa
Tinnakorn
T
Kusanovic
Juan Pedro
JP
Erez
Offer
O
Than
Nandor Gabor
NG
Hassan
Sonia S
SS
D000328:Adult; D020346:Aquaporins / Q000235:genetics* / Q000378:metabolism; D002821:Chorioamnionitis / Q000235:genetics* / Q000378:metabolism; D003430:Cross-Sectional Studies; D005321:Extraembryonic Membranes / Q000276:immunology / Q000378:metabolism*; D005260:Female; D005322:Premature Rupture of Fetal Membranes / Q000209:etiology / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D005865:Gestational Age; D006801:Humans; D007249:Inflammation / Q000235:genetics* / Q000378:metabolism; D007745:Labor Onset / Q000235:genetics* / Q000378:metabolism; D011247:Pregnancy; D047929:Term Birth / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D055815:Young Adult
C109669:AQP9 protein, human; D020346:Aquaporins