Cell cycle regulatory control for uterine stromal cell decidualization in implantation

Das, Sanjoy K.

doi:10.1530/rep-08-0539

Cited by 126 publications

(163 citation statements)

References 82 publications

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“…These results indicate that Tdo2 may be involved in mouse decidualization. Decidualization is a process which is characterized by uterine stromal cells proliferating and differentiating into decidual cells with polyploidy (Das 2009). This study showed that Tdo2 could regulate the proliferation of uterine stromal cells and decidual cells.…”

Section: Discussionmentioning

confidence: 99%

Differential expression and regulation of Tdo2 during mouse decidualization

Gao

Tian

et al. 2013

Journal of Endocrinology

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Tryptophan 2,3-dioxygenase (Tdo2) is a rate-limiting enzyme which directs the conversion of tryptophan to kynurenine. The aim of this study was to examine the expression and regulation of Tdo2 in mouse uterus during decidualization. Tdo2 mRNA was mainly expressed in the decidua on days 6-8 of pregnancy. By real-time PCR, a high level of Tdo2 expression was observed in the uteri from days 6 to 8 of pregnancy, although Tdo2 expression was observed on days 1-8. Simultaneously, Tdo2 mRNA was also detected under in vivo and in vitro artificial decidualization. Estrogen, progesterone, and 8-bromoadenosine-cAMP could induce the expression of Tdo2 in the ovariectomized mouse uterus and uterine stromal cells. Tdo2 could regulate cell proliferation and stimulate the expression of decidual marker Dtprp in the uterine stromal cells and decidual cells. Overexpression of Tdo2 could upregulate the expression of Ahr, Cox2, and Vegf genes in uterine stromal cells, while Tdo2 inhibitor 680C91 could downregulate the expression of Cox2 and Vegf genes in uterine decidual cells. These data indicate that Tdo2 may play an important role during mouse decidualization and be regulated by estrogen, progesterone, and cAMP.

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Section: Discussionmentioning

confidence: 99%

Differential expression and regulation of Tdo2 during mouse decidualization

Gao

Tian

et al. 2013

Journal of Endocrinology

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“…The initiation of implantation in mice is characterized by a localized increase in uterine vascular permeability at the site of the blastocyst attachment, which occurs in the midnight of day 4 of pregnancy and can be visible by intravenous injection of Chicago blue dye (blue reaction) [20]. Coincidently, stromal cells immediately surrounding the implanting blastocyst undergo extensive proliferation and subsequently differentiate into specialized cells that are polyploidy, and this process is known as decidualization [26]. This extensive cell proliferation and polyploidy event occurs in a well-organized manner.…”

Section: Uterine Physiological Role In Normal Reproductive Eventsmentioning

confidence: 99%

Determinants of uterine aging: lessons from rodent models

Kong

Zhang

Chen

et al. 2012

Sci. China Life Sci.

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The uterus is an indispensable organ for the development of a new life in eutherian mammals. The female mammalian reproductive capacity diminishes with age. In this respect, the senescence of uterine endometrium is convinced to contribute to this failure. This review focuses on the physiological function of the uterus and the related influence of aging mainly in rodent models. A better understanding of the underlying mechanisms governing the process of uterine aging is hoped to generate new strategies to prolong the reproductive lifespan in humans. . More importantly, this phenomenon of continuous decline of fecundity with age has also been confirmed in women over 35 years old [10][11][12]. The success of reproduction in eutherian mammals requires the uterus, a unique organ in the viviparity compared to other organisms ensuring full development of the new life in the maternal body [13]. The endometrial environment of uteri is proved to be one of the critical aspects to determine the reproductive capacity [14] and uterine factor has been proved to be critical for the decline of fecundity in both rodents and humans [4,15]. Most of the available information on uterine aging derives from studies on rats and mice [16]. In these species, life span is short and aging animal model can be easily established. This review focuses on the physiological function of the uterus and the related influence of aging mainly in rodent models. determinants, uterine aging, rodent models

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“…Underneath the epithelium, there is a loose connective tissue layer with stromal cells, glands, and blood vessels. Many uterine functions are under the regulation of ovarian steroid hormones, estrogens and progesterone (P 4 ; Dey et al 2004, Das 2009), and uterine cell types respond to hormones in a differential manner. Ovarian estrogen targets uterine epithelial cells, inducing proliferation and differentiation of these cells, whereas the proliferation of uterine stromal cells is under P 4 regulation.…”

Section: Introductionmentioning

confidence: 99%

“…Together, these hormones prepare the uterus for embryo implantation, a process that begins around midnight of day 4 of pregnancy. Thus, P 4 and estrogen are crucial regulators of cell cycle and cellular differentiation in the uterus (Das 2009). …”

Section: Introductionmentioning

confidence: 99%

Suppression of autophagic activation in the mouse uterus by estrogen and progesterone

Choi¹,

Shin²,

Song

et al. 2014

Journal of Endocrinology

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Autophagy is a major cellular catabolic pathway tightly associated with cell survival. The involvement of autophagy in the prolonged survival of blastocysts in the uterus is well established, and it was assumed that ovarian steroid hormones -progesterone (P 4 ) and estrogens -have important roles in the regulation of autophagy. However, information is scarce regarding whether these hormones regulate autophagy in certain hormoneresponsive cellular systems. In this study, we investigated the effects of estrogen and P 4 on autophagic response in the uteri of pregnant mice and in ovariectomized (OVX) mice treated with hormones. During pregnancy, autophagic response is high on days 1 and 2 when the uterus shows an inflammatory response to mating, but it subsides around the time of implantation. Dexamethasone treatment to day 1 pregnant mice reduced autophagy in the uterus. In OVX mouse uteri, estrogen or P 4 reduces autophagic response within 6 h. Glycogen content in OVX uteri was increased by 3-methyladenine treatment, suggesting that autophagy is involved in glycogen breakdown in the hormone-deprived uterus. The classical nuclear receptor antagonists, ICI 182 780 or mifepristone, lead to the recovery of the autophagic response in OVX uteri. The suppression of autophagy by 17b-estradiol is inversely correlated with the accumulation of phospho-mouse target of rapamycin, and rapamycin treatment is moderately effective in the upregulation of autophagic response in OVX mouse uteri. Collectively, this study establishes that the uterine autophagy is induced in hormone-derived environment and is suppressed by hormone treatment. Uterine autophagy may have multiple functions as a responsive mechanism to acute inflammation and as an energy provider by breaking down glycogen under hormone deprivation.

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Cell cycle regulatory control for uterine stromal cell decidualization in implantation

Cited by 126 publications

References 82 publications

Differential expression and regulation of Tdo2 during mouse decidualization

Differential expression and regulation of Tdo2 during mouse decidualization

Determinants of uterine aging: lessons from rodent models

Suppression of autophagic activation in the mouse uterus by estrogen and progesterone

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