Preimplantation maternal stress impairs embryo development by inducing oviductal apoptosis with activation of the Fas system

Zheng, Libing; Tan, Xiaodong; Cui, Xiang-Zhong; Yuan, Haiqing; Li, Hong; Jiao, Guiai; Ji, Chang-Li; Tan, Jing-He

doi:10.1093/molehr/gaw052

Cited by 27 publications

(20 citation statements)

References 62 publications

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“…Nevertheless, the embryo area under heat stress was 6.9% lower in thermal comfort conditions. Similar results have been showed by Edwards et al (1968) in gilts and Zheng et al (2016) in mice. The smaller embryonic size may have resulted from a lower embryonic and uterine luminal oestrogen concentration (Anderson et al 1993).…”

Section: Discussionsupporting

confidence: 89%

Exposure to high ambient temperatures alters embryology in rabbits

García

Argente

2017

Int J Biometeorol

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High ambient temperatures are a determining factor in the deterioration of embryo quality and survival in mammals. The aim of this study was to evaluate the effect of heat stress on embryo development, embryonic size and size of the embryonic coats in rabbits. A total of 310 embryos from 33 females in thermal comfort zone and 264 embryos of 28 females in heat stress conditions were used in the experiment. The traits studied were ovulation rate, percentage of total embryos, percentage of normal embryos, embryo area, zona pellucida thickness and mucin coat thickness. Traits were measured at 24 and 48 h post-coitum (hpc); mucin coat thickness was only measured at 48 hpc. The embryos were classified as zygotes or two-cell embryos at 24 hpc, and 16-cells or early morulae at 48 hpc. The ovulation rate was one oocyte lower in heat stress conditions than in thermal comfort. Percentage of normal embryos was lower in heat stress conditions at 24 hpc (17.2%) and 48 hpc (13.2%). No differences in percentage of zygotes or two-cell embryos were found at 24 hpc. The embryo development and area was affected by heat stress at 48 hpc (10% higher percentage of 16-cells and 883 μm smaller, respectively). Zona pellucida was thicker under thermal stress at 24 hpc (1.2 μm) and 48 hpc (1.5 μm). No differences in mucin coat thickness were found. In conclusion, heat stress appears to alter embryology in rabbits.

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Section: Discussionsupporting

confidence: 89%

Exposure to high ambient temperatures alters embryology in rabbits

García

Argente

2017

Int J Biometeorol

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“…Restraint stress impairs fertility in female mice through several mechanisms ( Figure 1 ). Mated female mice with elevated levels of glucocorticoids in response to restraint stress displayed pronounced apoptosis in the oviduct, poor embryo development, and fewer blastocysts per mouse [ 45 ]. Restraint stress in pregnant mice significantly reduced the pregnancy rate and average litter size of mice as compared to controls, attributed in part to reduced number of implantation sites [ 46 ].…”

Section: The Impacts Of Stress Throughout the Hpg Axismentioning

confidence: 99%

Stress and the HPA Axis: Balancing Homeostasis and Fertility

Joseph

Whirledge

2017

IJMS

189

110

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An organism’s reproductive fitness is sensitive to the environment, integrating cues of resource availability, ecological factors, and hazards within its habitat. Events that challenge the environment of an organism activate the central stress response system, which is primarily mediated by the hypothalamic–pituitary–adrenal (HPA) axis. The regulatory functions of the HPA axis govern the cardiovascular and metabolic system, immune functions, behavior, and reproduction. Activation of the HPA axis by various stressors primarily inhibits reproductive function and is able to alter fetal development, imparting a biological record of stress experienced in utero. Clinical studies and experimental data indicate that stress signaling can mediate these effects through direct actions in the brain, gonads, and embryonic tissues. This review focuses on the mechanisms by which stress activation of the HPA axis impacts fertility and fetal development.

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“…Previous studies in mice have reported that preimplantation restraint stress triggers apoptosis in oviducts, thereby leading to embryo mortality [14]. In our study, we quantified the amount of LDH, a cytoplasmic enzyme released to the cell environment when the plasma membrane is damaged during apoptosis, necrosis, and other forms of cellular damage, in both the apical secretion and basolateral medium after long-term cortisol stimulation [38].…”

Section: Discussionmentioning

confidence: 99%

“…In sows, stress evoked by food deprivation or repeated injection of adrenocorticotropic hormone (ACTH) during the postovulatory stage has been observed to lead to delayed ova transport, aberrant oviductal activity [9][10][11], endocrine profile changes, and impaired embryonic development [11]. Pregnant mice suffering from restraint stress during the embryonic oviduct transport period, as measured by elevated peripheral corticosterone levels (main rodent GC), have shown reduced embryo quality, conception rate, and litter size; furthermore, the negative consequences in this case were extended to behavior and physiology in postnatal life [12][13][14][15]. 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.…”

Section: Introductionmentioning

confidence: 99%

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

Trakooljul

Schoen

et al. 2020

IJMS

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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.

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Preimplantation maternal stress impairs embryo development by inducing oviductal apoptosis with activation of the Fas system

Cited by 27 publications

References 62 publications

Exposure to high ambient temperatures alters embryology in rabbits

Exposure to high ambient temperatures alters embryology in rabbits

Stress and the HPA Axis: Balancing Homeostasis and Fertility

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

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