Does Maternal Stress Affect the Early Embryonic Microenvironment? Impact of Long-Term Cortisol Stimulation on the Oviduct Epithelium

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.

Combined albumin and bicarbonate induces head-to-head sperm agglutination which physically prevents equine sperm–oviduct binding

In many species, sperm binding to oviduct epithelium is believed to be an essential step in generating a highly fertile capacitated sperm population primed for fertilization. In several mammalian species, this interaction is based on carbohydrate-lectin recognition.d-galactose has previously been characterized as a key molecule that facilitates sperm–oviduct binding in the horse. We used oviduct explant and oviduct apical plasma membrane (APM) assays to investigate the effects of various carbohydrates; glycosaminoglycans; lectins; S-S reductants; and the capacitating factors albumin, Ca2+and HCO3−on sperm–oviduct binding in the horse. Carbohydrate-specific lectin staining indicated thatN-acetylgalactosamine,N-acetylneuraminic acid (sialic acid) andd-mannose ord-glucose were the most abundant carbohydrates on equine oviduct epithelia, whereasd-galactose moieties were not detected. However, in a competitive binding assay, sperm–oviduct binding density was not influenced by any tested carbohydrates, glycosaminoglycans, lectins ord-penicillamine, nor did the glycosaminoglycans induce sperm tail-associated protein tyrosine phosphorylation. Furthermore,N-glycosidase F (PNGase) pretreatment of oviduct explants and APM did not alter sperm–oviduct binding density. By contrast, a combination of the sperm-capacitating factors albumin and HCO3−severely reduced (>10-fold) equine sperm–oviduct binding density by inducing rapid head-to-head agglutination, both of which events were independent of Ca2+and an elevated pH (7.9). Conversely, neither albumin and HCO3−nor any other capacitating factor could induce release of oviduct-bound sperm. In conclusion, a combination of albumin and HCO3−markedly induced sperm head-to-head agglutination which physically prevented stallion sperm to bind to oviduct epithelium.