Transcriptional Repression of Peri-Implantation EMX2 Expression in Mammalian Reproduction by HOXA10

Troy, Patrick; Daftary, Gaurang S.; Bagot, Catherine; Taylor, Hugh S.

doi:10.1128/mcb.23.1.1-13.2003

Cited by 120 publications

(100 citation statements)

References 56 publications

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“…Endometrial EMX2 expression is directly regulated by endogenous endometrial HOXA10. Normally EMX2 expression is downregulated in the peri-implantation period; however, this regulated expression fails in women with endometriosis (Troy et al 2003;Daftary and Taylor 2004). Further demonstrating the important role of this target gene, altering the endometrial Emx2 levels is not only associated with defective implantation, but also reduces litter size in mice .…”

Section: Hox Genes and Endometriosismentioning

confidence: 98%

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The Role ofHoxGenes in Female Reproductive Tract Development, Adult Function, and Fertility

Taylor

2015

Cold Spring Harb Perspect Med

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196

158

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HOX genes convey positional identity that leads to the proper partitioning and adult identity of the female reproductive track. Abnormalities in reproductive tract development can be caused by HOX gene mutations or altered HOX gene expression. Diethylstilbestrol (DES) and other endocrine disruptors cause Mü llerian defects by changing HOX gene expression. HOX genes are also essential regulators of adult endometrial development. Regulated HOXA10 and HOXA11 expression is necessary for endometrial receptivity; decreased HOXA10 or HOXA11 expression leads to decreased implantation rates. Alternation of HOXA10 and HOXA11 expression has been identified as a mechanism of the decreased implantation associated with endometriosis, polycystic ovarian syndrome, leiomyoma, polyps, adenomyosis, and hydrosalpinx. Alteration of HOX gene expression causes both uterine developmental abnormalities and impaired adult endometrial development that prevent implantation and lead to female infertility.

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Section: Hox Genes and Endometriosismentioning

confidence: 98%

“…The expression of EMX2 displayed a dynamic pattern that varied with the developmental phase of the human reproductive cycle ( Fig. 2) (Troy et al 2003).…”

Section: Hox Genes and Structure Of Female Reproductive Tractmentioning

confidence: 99%

The Role ofHoxGenes in Female Reproductive Tract Development, Adult Function, and Fertility

Taylor

2015

Cold Spring Harb Perspect Med

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196

158

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“…Embryonic endoderm gives rise to the bladder urothelium while the connective tissues and smooth muscle of the developing bladder are derived from the peri-cloacal mesenchyme (Haraguchi et al, 2007;Brenner-Anantharam et al, 2007). Genetic studies indicate the homeobox genes play an important role in determining the global patterning of the urogenital system (Satokata et al, 1995;Sciavolino et al, 1997;Warot et al, 1997;Goodman and Scambler, 2001;de Santa and Roberts, 2002;Troy et al, 2003), while key signaling molecules like sonic hedgehog and wnts have been implicated in determining the regional patterning within specific urogenital organs (Perriton et al, 2002;Freestone et al, 2003;Mericskay et al, 2004). The differentiation program responsible for the development of smooth muscle involves the complex interaction of epigenetic and genetic events including chromatin remodeling and acetylation, the SRF-myocar-din pathway, basic helix-loop-helix factors, AP-1 complex genes, and the ternary complex factors of the ETS domain family (Manabe and Owens, 2001;Chen et al, 2002;Du et al, 2003;Kumar and Owens, 2003;Miano, 2003;Wang et al, 2003Wang et al, , 2004Yoshida et al, 2003;Buchwalter et al, 2004;Spin et al, 2004;McDonald et al, 2006;Pipes et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Transcriptional profiling of the megabladder mouse: A unique model of bladder dysmorphogenesis

Singh¹,

Robinson²,

Ismail³

et al. 2007

Developmental Dynamics

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Recent studies in our lab identified a mutant mouse model of obstructive nephropathy designated mgb for megabladder. Homozygotic mgb mice (mgb؊/؊) develop lower urinary tract obstruction in utero due to a lack of bladder smooth muscle differentiation. This defect is the result of a random transgene insertion/translocation into chromosomes 11 and 16. Transcriptional profiling identified a significantly over-expressed cluster of gene products located on the translocated fragment of chromosome 16 including urotensin II-related peptide (Urp), which was shown to be preferentially over-expressed in developing mgb؊/؊ bladders. Pathway analysis of mgb microarray data indicated dysregulation of at least 60 gene products associated with smooth muscle development. In conclusion, the results of this study indicate that the molecular pathways controlling normal smooth muscle development are severely altered in mgb؊/؊ bladders, and provide the first evidence that Urp may play a critical role in bladder smooth muscle development. Developmental Dynamics 237:170 -186, 2008.

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“…In the adult mouse, Hoxa10 is expressed throughout the uterus, with the highest expression in the endometrium (Troy et al 2003). In normal mouse pregnancy, Hoxa10 expression can be seen on days 0.5 and 1.5 post-conception in the endometrium (Satokata et al 1995).…”

Section: Discussionmentioning

confidence: 95%

Identification of transcription factors at the site of implantation in the later stages of murine pregnancy

Zhao¹,

Koon²,

Bethin³

2006

Reproduction

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Despite medical advances, preterm delivery continues to complicate 12% of all births in the United States and is a major cause of neonatal deaths. One of the reasons that preterm labor continues to be a significant problem is that very little is understood about the factors involved in normal labor. Many investigators have studied parturition in the mouse and defined essential pathways for normal labor. Prostaglandins play an essential role in mouse labor and are important in human labor as well. We examined the 23 transcription factors from pregnant mouse uterus that change expression after the induction of cyclooxygenase-1, the enzyme that catalyzes the first committed step in prostaglandin synthesis. Using in situ hybridization, we have identified three of these transcription factors, Hoxa10, Hoxa11 and GILZ as being expressed in the decidua and regulated at the end of pregnancy. Both Hoxa10 and Hoxa11 are known to be critical for implantation, but very little is known about their roles in late gestation. GILZ has not previously been identified in the gravid uterus. In summary, we have identified three transcription factors that are regulated in the decidua at the end of pregnancy, suggesting a role in detachment of the fetus and placenta.

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Transcriptional Repression of Peri-Implantation EMX2 Expression in Mammalian Reproduction by HOXA10

Cited by 120 publications

References 56 publications

The Role ofHoxGenes in Female Reproductive Tract Development, Adult Function, and Fertility

The Role ofHoxGenes in Female Reproductive Tract Development, Adult Function, and Fertility

Transcriptional profiling of the megabladder mouse: A unique model of bladder dysmorphogenesis

Identification of transcription factors at the site of implantation in the later stages of murine pregnancy

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