BRG1 promotes<i>COUP-TFII</i>expression and venous specification during embryonic vascular development

Davis, Reema B.; Curtis, Carol D.; Griffin, Courtney T.

doi:10.1242/dev.087379

Cited by 61 publications

(63 citation statements)

References 47 publications

(78 reference statements)

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“…In addition, β-catenindependent and -independent pathways might regulate nr2f2 expression, as inhibition of β-catenin/Tcf-mediated transcription suppressed nr2f2 expression in the CV but not in the PCV. Consistent with this, the chromatin remodeling enzyme BRG1 directly promotes murine Nr2f2 expression independently of β-catenin (Davis et al, 2013). Furthermore, it was recently shown that nr2f2 expression in the PCV depends on Sox7 and Sox18 (Swift et al, 2014).…”

Section: Discussionmentioning

confidence: 52%

β-catenin-dependent transcription is central to Bmp-mediated formation of venous vessels

et al. 2015

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β-catenin regulates the transcription of genes involved in diverse biological processes, including embryogenesis, tissue homeostasis and regeneration. Endothelial cell (EC)-specific gene-targeting analyses in mice have revealed that β-catenin is required for vascular development. However, the precise function of β-cateninmediated gene regulation in vascular development is not well understood, since β-catenin regulates not only gene expression but also the formation of cell-cell junctions. To address this question, we have developed a novel transgenic zebrafish line that allows the visualization of β-catenin transcriptional activity specifically in ECs and discovered that β-catenin-dependent transcription is central to the bone morphogenetic protein (Bmp)-mediated formation of venous vessels. During caudal vein (CV) formation, Bmp induces the expression of aggf1, a putative causative gene for KlippelTrenaunay syndrome, which is characterized by venous malformation and hypertrophy of bones and soft tissues. Subsequently, Aggf1 potentiates β-catenin transcriptional activity by acting as a transcriptional co-factor, suggesting that Bmp evokes β-catenin-mediated gene expression through Aggf1 expression. Bmp-mediated activation of β-catenin induces the expression of Nr2f2 (also known as Coup-TFII), a member of the nuclear receptor superfamily, to promote the differentiation of venous ECs, thereby contributing to CV formation. Furthermore, β-catenin stimulated by Bmp promotes the survival of venous ECs, but not that of arterial ECs. Collectively, these results indicate that Bmp-induced activation of β-catenin through Aggf1 regulates CV development by promoting the Nr2f2-dependent differentiation of venous ECs and their survival. This study demonstrates, for the first time, a crucial role of β-catenin-mediated gene expression in the development of venous vessels.

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Section: Discussionmentioning

confidence: 52%

β-catenin-dependent transcription is central to Bmp-mediated formation of venous vessels

et al. 2015

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“…The mammalian SWITCH/sucrose nonfermentable (SWI/SNF)-like brahma-related gene 1 (BRG1), encoding an ATPase involved in chromatin remodeling, was found to promote the expression of COUP-TFII, and its inactivation resulted in the induction of arterial markers in veins. 52 In the fish, COUP-TFII has been recently reported to be a target of Sox7 and 18. 51 This, however, is in conflict with what was independently reported, whereby the knockdown of Sox7 and Sox18 would reduce arterial differentiation.…”

Section: Corada Et Al Specification Of Arteries and Veins 2375mentioning

confidence: 99%

Signaling Pathways in the Specification of Arteries and Veins

Corada

Morini

Dejana

2014

ATVB

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Abstract-The establishment of arterial and venous identity of endothelial cells is critical for the proper anatomic configuration and function of the vascular tree. Arterial and venous specification of endothelial cells is determined by genetic factors, although surrounding cells and hemodynamic forces may also contribute to vascular remodeling. This review provides an overview of the signaling pathways and related transcription factors implicated in differentiation of endothelial cells. We will discuss, in particular, the role of upstream and downstream effectors of Wnt, Sox, and Notch pathways.

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“…Indirectly, however, NR2F2 expression can be modulated by progesterone in the mouse uterus, through paracrine mechanisms involving epithelial cells and the HH pathway (Lee et al 2006b, Simon et al 2009b. Upstream regulators of NR2F2 expression must also be considered, including brahma-related gene 1 (SMARCA4 (BRG1)), which is a tumour suppressor that normally promotes NR2F2 expression (Davis et al 2013) and is induced by synthetic retinoids (Xu et al 2010). Interestingly, studies on SMARCA4 conditional homozygous mutants show that these mice develop uterine tumours (Serber et al 2012).…”

Section: Nr2f2 and Ctnnb1 In Uterine Fibroidsmentioning

confidence: 99%

Aberrant expression and regulation of NR2F2 and CTNNB1 in uterine fibroids

Zaitseva¹,

Holdsworth-Carson²,

Waldrip³

et al. 2013

Reproduction

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Uterine fibroids are the most common benign tumour afflicting women of reproductive age. Despite the large healthcare burden caused by fibroids, there is only limited understanding of the molecular mechanisms that drive fibroid pathophysiology. Although a large number of genes are differentially expressed in fibroids compared with myometrium, it is likely that most of these differences are a consequence of the fibroid presence and are not causal. The aim of this study was to investigate the expression and regulation of NR2F2 and CTNNB1 based on their potential causal role in uterine fibroid pathophysiology. We used real-time quantitative RT-PCR, western blotting and immunohistochemistry to describe the expression of NR2F2 and CTNNB1 in matched human uterine fibroid and myometrial tissues. Primary myometrial and fibroid smooth muscle cell cultures were treated with progesterone and/or retinoic acid (RA) and sonic hedgehog (SHH) conditioned media to investigate regulatory pathways for these proteins. We showed that NR2F2 and CTNNB1 are aberrantly expressed in fibroid tissue compared with matched myometrium, with strong blood vessel-specific localisation. Although the SHH pathway was shown to be active in myometrial and fibroid primary cultures, it did not regulate NR2F2 or CTNNB1 mRNA expression. However, progesterone and RA combined regulated NR2F2 mRNA, but not CTNNB1, in myometrial but not fibroid primary cultures.In conclusion, we demonstrate aberrant expression and regulation of NR2F2 and CTNNB1 in uterine fibroids compared with normal myometrium, consistent with the hypothesis that these factors may play a causal role uterine fibroid development.

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BRG1 promotesCOUP-TFIIexpression and venous specification during embryonic vascular development

Cited by 61 publications

References 47 publications

β-catenin-dependent transcription is central to Bmp-mediated formation of venous vessels

β-catenin-dependent transcription is central to Bmp-mediated formation of venous vessels

Signaling Pathways in the Specification of Arteries and Veins

Aberrant expression and regulation of NR2F2 and CTNNB1 in uterine fibroids

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