Leucine and arginine regulate trophoblast motility through mTOR-dependent and independent pathways in the preimplantation mouse embryo

González, Isabel Martín; Martin, Patrick; Burdsal, Carol A.; Sloan, Jennifer L.; Mager, Sela; Harris, Thurl E.; Sutherland, Ann

doi:10.1016/j.ydbio.2011.10.021

Cited by 91 publications

(91 citation statements)

References 114 publications

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“…This may be beneficial to embryonic and fetal growth and survival. Besides, in mouse embryo, arginine could regulate trophoblast motility through mTOR signaling pathway during the preimplantation period (González et al 2012). In our study, intrauterine injection of rapamycin during periimplantation period totally inhibited embryo implantation.…”

Section: Discussionsupporting

confidence: 47%

Arginine enhances embryo implantation in rats through PI3K/PKB/mTOR/NO signaling pathway during early pregnancy

Zeng¹,

Mao²,

Huang³

et al. 2013

Reproduction

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Our previous study has demonstrated that dietary arginine supplementation during early pregnancy enhanced embryo implantation in rats. However, the mechanism was not clear. The objective of this study was to determine the mechanism that arginine enhanced embryo implantation during early pregnancy. Rats were fed the basal diets supplemented with 1.3% (wt:wt) L-arginine-HCl or 2.2% (wt:wt) L-alanine (isonitrogenous control) once pregnancy. On d4 of pregnancy, rats were given intrauterine injection of L-NG-nitro arginine methyl ester (L-NAME, nitric oxide synthase inhibitor), a-difluoromethylornithine (DFMO, polyamine synthesis inhibitor), wortmannin (PI3K inhibitor), or rapamycin (mTOR inhibitor). On d7 of pregnancy, rats were killed. Intrauterine injection of L-NAME decreased the implantation sites, while dietary arginine supplementation increased the implantation sites. Intrauterine injection of DFMO decreased the pregnancy rate, which was reversed by dietary arginine supplementation. Intrauterine injection of rapamycin or wortmannin inhibited embryo implantation. However, dietary arginine supplementation did not reverse this inhibition. Western blot analysis revealed that the expression of uterine p-PKB and p-S6K1 was greater in rats fed the arginine-supplemented diet in the presence of L-NAME treatment compared with rats fed the control diet. In the presence of DFMO treatment, the expression of uterine iNOS and eNOS was significantly enhanced in the arginine group compared with the control group. Similarly, intrauterine injection of wortmannin or rapamycin decreased the expression of uterine iNOS and eNOS, which was enhanced by dietary arginine supplementation. These data indicated that dietary arginine supplementation during early pregnancy could enhance embryo implantation through stimulation of PI3K/PKB/mTOR/NO signaling pathway.

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Section: Discussionsupporting

confidence: 47%

Arginine enhances embryo implantation in rats through PI3K/PKB/mTOR/NO signaling pathway during early pregnancy

Zeng¹,

Mao²,

Huang³

et al. 2013

Reproduction

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“…The implantation process is initiated by blastocyst attachment to the receptive LE that occurs at midnight on day 3.5. Recent evidence suggests that there are two separate uterine signals regulating blastocyst implantation, one that primes the trophectoderm for attachment to the LE and another that initiates its motility, but the nature of those signals are not well defined (Gonzalez et al ., 2012). By day 5.5, the LE cells lining the implantation chamber and near the blastocyst undergo apoptosis allowing the motile trophectoderm to come into contact with stromal cells that are differentiating into decidual cells in a process that involves endoreduplication.…”

Section: Uterine Glands and Pregnancy In Micementioning

confidence: 99%

“…In adult rodents, blastocyst implantation defects arise from the loss of genes expressed specifically in the GE [LIF and calcitonin/calcitonin-related polypeptide, alpha (CALCA) (Stewart et al ., 1992, Zhu et al ., 1998)] as well as those in the LE and GE (i.e., Ihh, Klf5, Msx1/Msx2 ) (Daikoku et al ., 2011, Lee et al ., 2006, Wang and Dey, 2006) and LE and stroma (i.e., Ptgs2 ) (Lim et al ., 1999, Lim et al ., 1997). Of particular note, very few studies have evaluated the substances present in the ULF of mice (Daikoku et al ., 2005, Gonzalez et al ., 2012, Harris et al ., 2005). Given the cellular complexity of the uterus, analysis of the entire uterine transcriptome is not entirely advantageous given the preponderance of stroma and myometrium relative to the endometrial epithelia.…”

Section: Uterine Glands and Pregnancy In Micementioning

confidence: 99%

“…While progress has been made in understanding the regulation of uterine receptivity, the process of blastocyst activation itself remains poorly understood (Gonzalez et al ., 2012). Previous work indicates that AA play an important role in blastocyst activation (see (Martin et al ., 2003) for review).…”

Section: Biological Role Of Uterine Glands and Their Secretions In Immentioning

confidence: 99%

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Uterine glands: biological roles in conceptus implantation, uterine receptivity and decidualization

2014

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All mammalian uteri contain glands in the endometrium that synthesize or transport and secrete substances essential for survival and development of the conceptus (embryo/fetus and associated extraembryonic membranes). This review summarizes information related to the biological roles of uterine glands and their secretions in uterine receptivity, blastocyst/conceptus survival and implantation, and stromal cell decidualization. Studies with the ovine uterine gland knockout (UGKO) model support a primary role for uterine glands and, by inference, their secretions present in uterine luminal fluid histrotroph for conceptus survival and development. In rodents, studies with mutant and progesterone-induced UGKO mice found that uterine glands and their secretions are unequivocally required for establishment of uterine receptivity and blastocyst implantation and also may influence blastocyst trophectoderm activation and stromal cell decidualization in the uterus. Similarly in humans, histotroph from uterine glands appears critical for blastocyst implantation, uterine receptivity, and conceptus nutrition during the first trimester and uterine glands likely have a role in stromal cell decidualization. An increased understanding of uterine gland biology is important for diagnosis, prevention and treatment of fertility problems, particularly infertility and recurrent pregnancy loss, in domestic animals and humans.

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“…Recent evidence suggested that two separate uterine signals during blastocyst implantation. One signal primes the trophectoderm for attachment to the luminal epithelium, and the other results in the uptake of amino acids by the blastocyst, the motility of which is initiated for invasion (Gonzalez 2012). Signaling of endometrial receptivity to blastocyst attachment involves the actions of ovarian steroid hormones on the luminal epithelia and paracrine factors expressed by different endometrial cell types (Cha et al 2012, Zhang et al 2013.…”

Section: Retinoid Signaling In Blastocyst Implantationmentioning

confidence: 99%

Physiological and pathological implications of retinoid action in the endometrium

Jiang

Chen

Taylor

et al. 2018

Journal of Endocrinology

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Retinol (vitamin A) and its derivatives, collectively known as retinoids, are required for maintaining vision, immunity, barrier function, reproduction, embryogenesis and cell proliferation and differentiation. Despite the fact that most events in the endometrium are predominantly regulated by steroid hormones (estrogens and progesterone), accumulating evidence shows that retinoid signaling is also involved in the development and maintenance of the endometrium, stromal decidualization and blastocyst implantation. Moreover, aberrant retinoid metabolism seems to be a critical factor in the development of endometriosis, a common gynecological disease, which affects up to 10% of reproductive age women and is characterized by the ectopic localization of endometrial-like tissue in the pelvic cavity. This review summarizes recent advances in research on the mechanisms and molecular actions of retinoids in normal endometrial development and physiological function. The potential roles of abnormal retinoid signaling in endometriosis are also discussed. The objectives are to identify limitations in current knowledge regarding the molecular actions of retinoids in endometrial biology and to stimulate new investigations toward the development potential therapeutics to ameliorate or prevent endometriosis symptoms.

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Leucine and arginine regulate trophoblast motility through mTOR-dependent and independent pathways in the preimplantation mouse embryo

Cited by 91 publications

References 114 publications

Arginine enhances embryo implantation in rats through PI3K/PKB/mTOR/NO signaling pathway during early pregnancy

Arginine enhances embryo implantation in rats through PI3K/PKB/mTOR/NO signaling pathway during early pregnancy

Uterine glands: biological roles in conceptus implantation, uterine receptivity and decidualization

Physiological and pathological implications of retinoid action in the endometrium

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