Abstract
Maternal stress before or during the sensitive preimplantation phase is associated with reproduction failure. Upon real or perceived threat, glucocorticoids (classic stress hormones) as cortisol are synthesized. The earliest “microenvironment” of the embryo consists of the oviduct epithelium and the oviductal fluid generated via the epithelial barrier. However, to date, the direct effects of cortisol on the oviduct are largely unknown. In the present study, we used a compartmentalized in vitro system to test the hypothesis that a prolonged stimulation with cortisol modifies the physiology of the oviduct epithelium. Porcine oviduct epithelial cells were differentiated at the air–liquid interface and basolaterally stimulated with physiological levels of cortisol representing moderate and severe stress for 21 days. Epithelium structure, transepithelial bioelectric properties, and gene expression were assessed. Furthermore, the distribution and metabolism of cortisol was examined. The polarized oviduct epithelium converted basolateral cortisol to cortisone and thereby reduced the amount of bioactive cortisol reaching the apical compartment. However, extended cortisol stimulation affected its barrier function and the expression of genes involved in hormone signaling and immune response. We conclude that continuing maternal stress with long-term elevated cortisol levels may alter the early embryonic environment by modification of basic oviductal functions.
Highlights
The beginning of life takes place in the oviduct, which is called the “fallopian tube”
The earliest “microenvironment” of the embryo consists of the oviduct epithelium and the oviductal fluid generated via the epithelial barrier
The “microenvironment” of the early embryo consists of the oviduct epithelium, and the oviductal fluid generated via active epithelium secretion as well as passive and active transport across the epithelial barrier
Summary
The beginning of life takes place in the oviduct, which is called the “fallopian tube”. In vitro studies which exclude actions through the nervous system have revealed that zygotes co-cultured with mouse oviductal epithelial cells treated with high doses of corticosterone or corticotropin-releasing hormone (CRH) show reduced developmental competence (decreased blastocyst rate and blastocysts with decreased numbers of blastomeres) [16], while direct corticosterone/CRH exposure to mouse zygotes does not compromise embryo development. This altogether suggests that the effect of maternal GC on early embryos might be transmitted indirectly by the oviduct [16]. The extracellular environment was examined from both apical and basal compartments for markers of cell damage, distribution, and metabolism of cortisol and cortisone
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