Disease relevance of Deciduoma

• MPA treatment was found to induce uterine secretory changes, glandular cystic hyperplasia, and eventually deciduomas that stained strongly for desmin and to a lesser degree for vimentin, suggesting a muscular differentiation [1].

High impact information on Deciduoma

• Increased concentrations of apoptotic cells were observed at the periphery of the growing deciduoma and in the antimesometrial deciduoma near the luminal epithelium after both treatments [2].
• In vitro, murine decidual cells derived from artificially induced deciduomas could be induced to produce the Isg15 protein as well as Isg15-conjugated proteins when stimulated with type 1 IFN, though were less responsive to IFN-gamma [3].
• Furthermore, our observations support the hypothesis that the expression of IGFBP-1, a protein capable of inhibiting the mitogenic activity of IGF-I, in deciduoma tissue may inhibit paracrine IGF-1 actin and allow for the differentiation of stromal tissue [4].
• Mechanical separation of the deciduoma tissue from the underlying myometrium revealed that the deciduoma tissue was depleted in IGF-I mRNA, while the majority of the IGFBP-1 was located in the deciduoma tissue [4].
• This strongly suggests a close relationship between the loss of PR and the regression of the deciduoma [5].

Biological context of Deciduoma

• Prostaglandin, dehydrogenase activity was determined in deciduomal and myometrial tissues during growth and regression of the deciduoma during pseudopregnancy [6].
• Content of the thiobarbituric acid reactive substances (TBARS) as well as lipid peroxidation induced by ascorbate and cumene hydroperoxide showed significant decreases during deciduoma growth [7].

Anatomical context of Deciduoma

• These results suggest that mast cells are not essential for formation of deciduomata and that histamine originating from sources other than mast cells may be important in deciduoma formation [8].
• However, the decidual expression of cyclin D3 mRNA was not dependent on the presence of blastocysts, since increased expression also occurred in experimentally induced deciduoma in the absence of blastocysts [9].
• The results suggest that the factors synthetised by decidua or deciduoma are the same and are not induced by exposure to foreign histocompatibility antigens of the fetus [10].
• Expression of parathyroid hormone-related protein (PTHrP) and the PTH/PTHrP receptor in the rat uterus during early pregnancy and following artificial deciduoma induction [11].
• 6. These results indicate that, in the endometrium, the iNOS/endogenous nitric oxide system may be linked to the biochemical and metabolic mechanisms responsible for the developmental responsiveness of the deciduoma to dexamethasone exposure [12].

Associations of Deciduoma with chemical compounds

• Inhibitory effects of aminoglutethimide and isoxazole on progesterone production and deciduoma formation in rats [13].
• Serum progesterone levels were determined, and the changes of estrogen and progesterone receptors (ER and PR, respectively) were simultaneously studied in the deciduoma [5].
• The rise and fall in E2 and P receptors during the earlier stages of deciduoma differentiation confirmed the work of others [14].
• Prostaglandin dehydrogenase activity for both prostaglandin E1 (PGE1) and prostaglandin F2alpha (PGF2alpha) in deciduomal and myometrial tissues increased during the growth of the deciduoma and decreased during the regression phase [6].
• Northern blot analysis of RNA from the deciduoma produced in ovariectomized, steroid-treated rats by intrauterine injection of oil demonstrated a similar temporal pattern of expression of uPA mRNA; i.e., the level of uPA mRNA was highest on Day 7 and decreased thereafter [15].

Gene context of Deciduoma

• Consistent with angiogenesis in general during decidualization, we believe EDG1 and EDG5 to be regulated by the embryo because no microvascular expression for these receptors was observed in oil-induced deciduomas [16].
• Maternal TIMP-3 expression also occurred in the absence of embryonic MMP-9 expression in decidual reactions induced by parthenogenetic embryos (where MMP-9 positive cells were not detected) or in oil-induced deciduomas [17].
• In contrast, MT-III and MT-IV mRNAs were both abundant in the maternal deciduum, and in experimentally induced deciduoma on 7 and 8 days postcoitum (1 dpc = vaginal plug), as are MT-I and -II mRNAs [18].
• Severe trauma, such as crushing of the uterine tissue, has previously been shown to remove the requirement for nidatory estradiol for deciduomas to develop, indicating that the greater susceptibility of alphaERKO uterine tissue to damage from intraluminal oil infusion is contributing to decidualization in the absence of ERalpha [19].
• Although the artificially-induced deciduoma weights and number of implantation sites were similar between stathmin-knockout (KO) and wild-type (WT) mice, the stathmin-KO mice had fewer newborn pups (reduced by 30%) [20].

Analytical, diagnostic and therapeutic context of Deciduoma

• Northern blot analysis demonstrated TGF-alpha mRNA expression specifically in the deciduoma beginning on the day of decidual stimulus (Day 4), increasing on Day 6, and continuing through Day 14 [21].
• With respect to progestomimetic activity in vivo, trimegestone was more potent than reference progestins in the endometrial transformation test in the rabbit, preventing the uterotrophic effect of estradiol in the immature mouse bioassay, and had more effect on traumatic deciduoma formation and greater oral antiovulatory activity in the rat [22].

References