Presence of Urokinase Plasminogen Activator and Plasminogen Activator Inhibitor-1 Messenger Ribonucleic Acids in Rat Endometrium during Decidualization in Vivo1

Wang, Shuli; Kennedy, T. G.; Zhang, Xingqi

doi:10.1095/biolreprod55.3.493

Cited by 21 publications

(12 citation statements)

References 35 publications

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“…Plasmin is able to degrade most of the components of the ECM either directly or indirectly by the activation of MMPs. All of the plasminogen/plasmin factors mentioned previously participate in the process of decidualization [19-21]. …”

Section: Discussionmentioning

confidence: 99%

“…It is synthesized as an inactive precursor (preproendothelin) and processed to a mature active form (endothelin) by zinc metalloproteinases. The active form, endothelin-1, promotes synthesis of collagen types I and II by fibroblasts, affects the ECM remodelling and promotes the proliferation of mesangial cells [21]. Endothelin-1 is also associated with neovascularization and regulation of blood flow [22].…”

Section: Discussionmentioning

confidence: 99%

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Callegari

Ferguson-Gottschall

Gibori

2005

Reprod Biol Endocrinol

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In the rat, the decidual tissue is an important component for maternal recognition of pregnancy. Decidualization can be induced by either the implantation of the blastocyst or by artificial stimuli. The process of decidua formation or decidualization, is characterized by growth and differentiation of endometrial stromal cells. Prostaglandin F2alpha (PGF2α) has been shown to be involved in inhibition of implantation, alteration of embryo development, induction of luteal regression, and the mediation of pregnancy loss induced by microorganism infections. In order to establish a direct role for PGF2α in decidual function, we have evaluated its effects on the expression of an extensive array of genes using primary decidual cell culture. Upon treatment with PGF2α sixty genes were significantly down-regulated whereas only six genes were up-regulated (from a total of 1176 genes studied). Interestingly, the majority of the genes inhibited by PGF2α are either directly or indirectly involved in the turnover of the extracellular matrix (ECM). Genes such as gelatinase A (MMP2), cathepsin L, tissue inhibitor metalloproteinases 2 (TIMP2) and 3 (TIMP3), plasminogen activator inhibitor1 (PAI1), tissue type plasminogen activator (tPA), urokinase plasminogen activator (tPA), endothelin 1, calponin, carboxypeptidase D and calponin acidic were down regulated. The opposite effect was observed for prostromelysin 53 kDa (proMMP3), plasma proteinase I alpha and alpha 1 antiproteinase, all of which were significantly up-regulated by PGF2α. The results strongly suggest that the abortificient role of elevated levels of PGF2α after implantation is due, in large part, to inhibition of genes involved in the normal turnover of the extracellular matrix necessary for decidual formation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Untitled

Callegari

Ferguson-Gottschall

Gibori

2005

Reprod Biol Endocrinol

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“…These values from several gels were then pooled to calculate the means and SEM for each day of pregnancy. Duncan's Multiple Range test was used to determine the statistical significance of differences between values [17]. In some experiments, the complete implantation complexes (uterine implantation site and the placenta) were collected on the days indicated and processed together; in other experiments, the uterine implantation site and the placenta were processed separately.…”

Section: Northern Blot Analysismentioning

confidence: 99%

Spatio-Temporal Pattern for Expression of Galectin-3 in the Murine Utero-Placental Complex: Evidence for Differential Regulation1

Lee¹,

Lee²,

Phillips³

et al. 1998

Biology of Reproduction

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In mice, immunoreactive galectin-3 protein has previously been localized in uterine epithelial cells adjacent to implanting blastocysts as well as in the decidualized endometrium of implantation sites, uterine natural killer cells, and several types of placental trophoblast cells. Because galectin-3 is a soluble extracellular molecule, protein localization by immunohistochemical methods does not demonstrate its cellular origin. Therefore, the present study was undertaken to determine precisely which cell types in the utero-placental complex express galectin-3 mRNA. In situ hybridization results demonstrated that galectin-3 mRNA was expressed throughout the utero-placental complex in all cell types previously shown to contain immunoreactive protein, including uterine epithelium, decidualized endometrium, uterine natural killer cells, and placental trophoblasts. These results indicate that galectin-3 protein is not synthesized in a restricted cell type and translocated through the extracellular spaces to other tissue compartments. Furthermore, Northern blot analysis of total RNA prepared from separated fetal and maternal components of utero-placental complexes demonstrated different patterns of expression for galectin-3 mRNA in the uterus and placenta. Relative levels of galectin-3 mRNA peak at midgestation in the implantation site and during the second half of gestation remain elevated in the placenta but decline in the uterus. Separate mechanisms for regulating expression of galectin-3 on opposite sides of the feto-maternal interface are indicated.

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“…The PAs cleave plasminogen to plasmin, which degrades ECM components such as fibronectin and laminin, and are activators of MMPs; their natural inhibitors are the plasminogen activator inhibitors. Transcripts for uPA, tPA, and plasminogen activator inhibitor-1 have all been detected within the uterus during decidualization both in vivo and in vitro (50,51). PGE 2 and EGF increase levels for uPA, but not tPA (51,52), providing additional evidence that EGF increases the proteolytic activity of stromal cells in vitro.…”

Section: Discussionmentioning

confidence: 89%

Epidermal Growth Factor and Basic Fibroblast Growth Factor Increase the Production of Matrix Metalloproteinases during in Vitro Decidualization of Rat Endometrial Stromal Cells

Nuttall

Kennedy

2000

Endocrinology

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Numerous growth factors are involved in mediating proliferation and differentiation of endometrial stromal cells during decidualization. During this period, the extracellular matrix of the endometrium undergoes extensive remodeling. We tested the hypothesis that epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), and transforming growth factor-␤ regulate expression of matrix metalloproteinases (MMPs) and their inhibitors, tissue inhibitors of metalloproteinases (TIMPs), during decidualization. Stromal cells were isolated from uteri hormonally sensitized to undergo decidualization and were cultured in the absence or presence of a growth factor. Using substrate-gel electrophoresis with gelatin as the substrate, we detected activity for gelatinase A and B, and collagenase-3, and using casein as a substrate, we detected activity for stromelysin-1. Increasing concentrations of EGF and bFGF resulted in increased activity of gelatinase B, collagenase-3, and stromelysin-1. Northern blot analyses revealed that EGF and bFGF also increased messenger RNA levels for these MMPs. There was no effect of these growth factors on gelatinase or TIMP-1, -2, and -3, nor was there an effect of transforming growth factor-␤ on any MMP or TIMP examined. These data demonstrate that EGF and bFGF increase levels of proteolytic enzymes produced by endometrial stromal cells undergoing decidualization in vitro while having no effect on their inhibitors. (Endocrinology 141: 629 -636, 2000) D URING EMBRYO implantation in rodents, the stromal fibroblast cells of the endometrium proliferate and differentiate into decidual cells, a process that ultimately results in the formation of the maternal component of the placenta (1). Several lines of evidence indicate that this process, in addition to being regulated by estrogen and progesterone, is also regulated by several locally produced growth factors. There is increased binding of epidermal growth factor (EGF) to the uterus during decidualization (2), and this factor is able to induce embryo implantation in the absence of estrogen (3). The messenger RNA (mRNA) for basic fibroblast growth factor (bFGF) is present in the uterus during early pregnancy (4), and its levels increase substantially during decidualization, specifically within the mesometrial decidual cells (5). The expression of bFGF in the uterus is regulated by progesterone, and bFGF is involved in controlling both stromal cell proliferation (6) and angiogenesis (5). The mRNA for transforming growth factor-␤ (TGF␤) is also present within the uterus during pregnancy and is localized to the luminal and glandular epithelial cells during early decidualization and to macrophages during midgestation (7).During decidualization, the extracellular matrix (ECM) of the endometrium undergoes extensive remodeling, whereby the fibrillar collagen underlying the undifferentiated stromal cells becomes less fibrous due to the removal of several collagen components from the matrix (8). Subsequently, the newly differentiated decidu...

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Presence of Urokinase Plasminogen Activator and Plasminogen Activator Inhibitor-1 Messenger Ribonucleic Acids in Rat Endometrium during Decidualization in Vivo1

Cited by 21 publications

References 35 publications

Untitled

Untitled

Spatio-Temporal Pattern for Expression of Galectin-3 in the Murine Utero-Placental Complex: Evidence for Differential Regulation1

Epidermal Growth Factor and Basic Fibroblast Growth Factor Increase the Production of Matrix Metalloproteinases during in Vitro Decidualization of Rat Endometrial Stromal Cells

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