Dysregulation of hydrogen sulphide metabolism impairs oviductal transport of embryos.

Abstract

Embryo retention in the fallopian tube is thought to lead to ectopic pregnancy, which is a significant cause of morbidity. Hydrogen sulphide (H2S) is a gaseotransmitter produced mainly by cystathionine-γ-lyase and cystathionine-β-synthase. Here we show that cystathionine-γ-lyase and cystathionine -β-synthase are ubiquitously distributed in human fallopian tube epithelium and that H2S signalling relaxes the spontaneous contraction of the human oviduct. Furthermore, an aberration in H2S signalling, either silenced or enhanced activity induced by pharmacologic or genetic methods, causes embryo retention and developmental delay in the mouse oviduct, which is partly reversed by administration of either GYY4137, a slow-releasing H2S donor, or NaHS. Our findings reveal a new regulatory mechanism for oviductal embryo transport.