A physiological, rather than a superovulated, post‐implantation environment can attenuate the compromising effect of assisted reproductive techniques on gene expression in developing mice embryos

Bonakdar, Elham; Edriss, M. A.; Bakhtari, Azizollah; Jafarpour, Farnoosh; Asgari, V.; Hosseini, Sayyed Morteza; Boroujeni, N. Sadeghi; Hajian, Mehdi; Rahmani, Hamidreza; Nasr-Esfahani, Mohammad Hossein

doi:10.1002/mrd.22461

Cited by 19 publications

(20 citation statements)

References 80 publications

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“…In contrast to previous reports, 8,27,44 we show here that VDD alone (without hypocalcemia) did not reduce sperm cell motility, regardless of the severity of VDD. We therefore reinforce the idea that the previously reported reduction in sperm motility in VDD cases was likely a calcium‐mediated effect, as suggested 8,27‐49 . The results of our experiments are therefore in complete agreement with Sun et al 27 who demonstrated that VDD is accompanied by decreased extracellular calcium and phosphorus levels and that defective sperm motility in these situations can be overcome by calcium and phosphorus supplements.…”

Section: Discussionsupporting

confidence: 93%

Impact of vitamin D deficiency on mouse sperm structure and function

et al. 2020

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Background In rodents and humans, vitamin D deficiency (VDD) is associated with altered sperm structure and function (primarily decreased motility and morphological abnormalities) that are primarily attributed to VDD‐induced hypocalcemia. However, it is suspected that VDD has much more drastic effects on mammalian spermatozoa. Objectives The purpose of this study was to illustrate that VDD, depending on its severity and duration, can alter sperm nuclear integrity and can also lead to the loss of spermatozoa's ability to support embryonic development. Materials and methods A mouse model of induced VDD combining the action of a vitamin D‐deficient diet, UV exposure limitation, and paricalcitol injections; a vitamin D2 analog that catabolizes endogenous vitamin D by increasing the expression of CYP24A, a member of the cytochrome P450 family, has been used to create different grades of VDD. Results We show that the most significant sperm defect recorded concerns the integrity of the paternal nucleus, which is both decondensed and fragmented in moderate‐to‐severe VDD situations. Consistent with the known consequences of fertilization with DNA‐damaged spermatozoa, we show that paternal VDD decreases the ability of spermatozoa to optimally support fertilization and embryonic development. Discussion and Conclusion Given the worldwide high prevalence of VDD in humans, and although obtained in an animal model, the data presented here suggest that subfertile/infertile males may benefit from VDD testing and that attempts to correct serum vitamin D levels could be considered prior to conception, either naturally or through ART.

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Section: Discussionsupporting

confidence: 93%

Impact of vitamin D deficiency on mouse sperm structure and function

et al. 2020

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“…In cows, treatments with gonadotropins resulted in altered oocyte LD accumulation and blastocyst development, expression of genes that regulate metabolic activity of the embryo, serum profile of P4 and PG metabolites, milk E2 concentration, endometrial and embryonic gene expression, and uterine blood flow, secretory functions, morphology and vascular density [43][44][45][80][81][82][83][84]. In mice, some adverse effects of gonadotropin treatments on blastocyst and conceptus gene expression, fetal development and and lower implantation and pregnancy rates have also been demonstrated [85,86]. In the present study, FSH enhanced expression of LDs in LE and EG in O and/or U at the mid-luteal phase, in fact restoring LD expression to control levels.…”

Section: Revised 12mentioning

confidence: 99%

Lipid droplets in the ovine uterus during the estrous cycle: Effects of nutrition, arginine, and FSH

et al. 2017

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The aim of this study was to evaluate lipid droplet (LD) expression in uteri of FSH-treated or nontreated sheep administered with arginine (Arg) or vehicle (saline, Sal) and fed a control (C), excess (overfed, O) or restricted (underfed, U) diet. In experiment 1, ewes from each diet were randomly assigned to Arg or Sal treatments administered three times daily starting on Day 0 of the first estrous cycle until blood sample and uterine tissue collection at the early- or mid-luteal phase of the second estrous cycle or the late-luteal phase of the first estrous cycle. In experiment 2, ewes were injected twice daily with FSH on Days 13 to 15 of the first estrous cycle, and blood samples and uterine tissue were collected at the early- and mid-luteal phases of the second estrous cycle. Cryopreserved in optimum cutting temperature (OCT) compound, cross-sections of uterine horn were stained with boron-dipyrromethene (BODIPY; marker of LDs) followed by 4',6-diamidino-2-phenylindole (DAPI) staining and image analysis to determine the proportion (%) of area occupied by LD in luminal epithelium (LE) and endometrial glands (EGs). Control ewes maintained, O ewes gained, and U ewes lost body weight during the experiments. Serum progesterone concentration was not affected by nutritional plane or Arg treatment and was 5.5-fold greater in FSH- than Sal-treated ewes. LDs were detected in LE and superficial EG (close to LE) but not deep EG, or other uterine compartments, and area occupied by LD was greater in LE than in EG. In experiment 1, in LE and EG, area occupied by LDs was greater in C than in O or U; greater in Arg than in Sal; and greater at the late-, less at mid-, and least at early-luteal phases. In experiment 2, in LE and EG, area occupied by LDs was greater at mid- than in early-luteal phase. Comparison of data from FSH-treated and nontreated ewes (e.g., experiment 1 vs. experiment 2) demonstrated that FSH increased the area occupied by LD in LE and EG regardless of diet. Interactions between FSH treatment, stage of the estrous cycle, and plane of nutrition demonstrated that FSH increased the area occupied by LD in LE and EG at the mid-luteal phase in O and U. Thus, LDs are differentially distributed in uterine compartments, and area occupied by LD in endometrium is affected by nutritional plane, Arg or FSH, and stage of the estrous cycle. Such changes in dynamics of LD in the endometrium during the estrous cycle indicate their specific role in uterine functions.

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“…Ovarian stimulation is performed to obtain a high number of oocytes during a defined ovarian cycle by administering gonadotropins. In ovarian stimulation, exogenous luteinizing hormone and follicle‐stimulating hormone are used, and thus in a single cycle, many follicles begin to grow and eventually ovulate (Bonakdar et al, ). Preparing the endometrium for implantation requires proper hormonal stimulation (Macklon, Stouffer, Giudice, & Fauser, ).…”

Section: Introductionmentioning

confidence: 99%