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Carbon monoxide attenuates bacteria-induced Endothelin-1 expression in second trimester placental explants.

Abstract：

INTRODUCTION:The pro-inflammatory mediator and potent vasoconstrictor Endothelin-1 (ET-1) is known to be expressed in the placenta. We have recently demonstrated that very low, non-toxic doses of carbon monoxide (CO), prevented infection-induced preterm birth in mice. However the effect(s) of CO on human gestational tissues is yet to be fully explored. We hypothesize that CO will have a protective role against inflammation-induced E. coli by down-regulating the ET axis in placental explants. METHODS:Twenty placentas from elective termination of pregnancy in the second trimester were analyzed with or without exposure to heat killed E. coli over the course of 30 h. Placental ET-1, along with its biologically inactive precursor Big ET-1, and Endothelin Converting Enzyme-1 (ECE-1, responsible for the cleavage of Big ET-1 to ET-1), were analyzed by ELISA. Gene expression for ET-1 (EDN1), ECE-1 and the ETA receptor (EDNRA) were analyzed using qPCR. Localization of ET-1 expression was also demonstrated using immunohistochemistry. RESULTS:E. coli significantly increased ET-1 transcription and secretion of BIG ET-1 and ET-1 in a time dependant manner which was ameliorated when exposed to CO at later time points. In the presence of CO, mRNA levels of ECE-1 were significantly reduced at 3 and 24 h, while EDNRA was significantly reduced at 6 and 18 h. CONCLUSIONS:Up-regulation of ET-1 production in human placenta in the setting of infection can be attenuated by low doses of CO. Our results further explore the anti-inflammatory and regulatory mechanism(s) of CO on the ET axis components at the maternal fetal interface.

journal_name

Placenta

journal_title

Placenta

authors

Olgun NS,Arita Y,Hanna M,Murthy A,Tristan S,Peltier MR,Hanna N

doi

10.1016/j.placenta.2014.03.015

subject

Has Abstract

pub_date

2014-06-01 00:00:00

pages

351-8

issue

6

eissn

0143-4004

issn

1532-3102

pii

S0143-4004(14)00124-6

journal_volume

35

pub_type

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