The Ets1 proto-oncogene is upregulated by retinoic acid: characterization of a functional retinoic acid response element in the Ets1 promoter

Raouf, Afshin; Li, Vincent; Kola, Ismail; Watson, Dennis K.; Seth, Arun

doi:10.1038/sj.onc.1203505

Cited by 31 publications

(25 citation statements)

References 32 publications

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“…Hydrogen peroxide, a well known pro-angiogenic stimulus (44,45), activates nuclear factor (erythroid-derived 2)-like 2, leading to binding to antioxidant response elements and subsequent enhancement of Ets-1 promoter activity (46). Retinoic acid induces angiogenesis (47), with concomitant induction of Ets-1 transactivation (48). The findings from the current investigation, which agree with our previously published work (3), suggest an additional mechanism: Ets-1 expression is regulated through post-transcriptional modification in response to angiogenic stimulation.…”

Section: Discussionsupporting

confidence: 82%

The MicroRNA miR-199a-5p Down-regulation Switches on Wound Angiogenesis by Derepressing the v-ets Erythroblastosis Virus E26 Oncogene Homolog 1-Matrix Metalloproteinase-1 Pathway

Chan

Roy

Huang

et al. 2012

Journal of Biological Chemistry

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Background:The role of miR-199a-5p in angiogenesis remains unclear. Results: miR-199a-5p exerts angiostatic effects by targeting Ets-1-MMP1 pathway and is down-regulated in skin wound healing. Conclusion: Down-regulation of miR-199a-5p switches on wound angiogenesis through derepressing of Ets-1-MMP1 pathway. Significance: This investigation provides novel mechanistic insight explaining miR-dependent regulation of wound angiogenesis and the foundation of developing therapeutic intervention in treating chronic nonhealing wounds.

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Section: Discussionsupporting

confidence: 82%

The MicroRNA miR-199a-5p Down-regulation Switches on Wound Angiogenesis by Derepressing the v-ets Erythroblastosis Virus E26 Oncogene Homolog 1-Matrix Metalloproteinase-1 Pathway

Chan

Roy

Huang

et al. 2012

Journal of Biological Chemistry

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“…In this search for osteogenic cells, we restricted our analysis to the nonhematopoietic (CD45 Ϫ Ter119 Ϫ ) subset of boneassociated cells, 2,6,9,10 and screened this subset for expression of osteoblast-associated cell surface markers ( Figure 1B and data not shown). Given that previous studies have demonstrated relatively restricted expression by bone lineage cells of the secreted/cell surface marker osteopontin (OPN), [30][31][32][33][34][35][36] and that analyses of OPN Ϫ/Ϫ mice suggest that OPN acts on HSCs to restrict their numbers in vivo, 8,37 we hypothesized that OPN might serve as a useful marker for the identification and isolation of HSCinteracting osteoblastic niche cells. Indeed, flow cytometric analysis revealed the existence of a distinct population of nonhematopoietic (CD45 Ϫ Ter119 Ϫ ) cells expressing OPN (OPN ϩ ), which was present in preparations of enzymatically liberated bone-associated cells but was not detected among BM cells ( Figure 1B).…”

Section: Osteoblasts Can Be Isolated By Direct Cell Sortingmentioning

confidence: 99%

Osteolineage niche cells initiate hematopoietic stem cell mobilization

Mayack

Wagers

2008

Blood

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Recent studies have implicated bonelining osteoblasts as important regulators of hematopoietic stem cell (HSC) self-renewal and differentiation; however, because much of the evidence supporting this notion derives from indirect in vivo experiments, which are unavoidably complicated by the presence of other cell types within the complex bone marrow milieu, the sufficiency of osteoblasts in modulating HSC activity has remained controversial. To address this, we prospectively isolated mouse osteoblasts, using a novel flow cytometry-based approach, and directly tested their activity as HSC niche cells and their role in cyclophosphamide/granulocyte colony-stimulating factor (G-CSF)-induced HSC proliferation and mobilization. We found that osteoblasts expand rapidly after cyclophosphamide/G-CSF treatment and exhibit phenotypic and functional changes that directly influence HSC proliferation and maintenance of reconstituting potential. Effects of mobilization on osteoblast number and function depend on the function of ataxia telangiectasia mutated (ATM), the product of the Atm gene, demonstrating a new role for ATM in stem cell niche activity. These studies demonstrate that signals from osteoblasts can directly initiate and modulate HSC proliferation in the context of mobilization. This work also establishes that direct interaction with osteolineage niche cells, in the absence of additional environmental inputs, is sufficient to modulate stem cell activity. (Blood. 2008;112:519-531) IntroductionMature blood cells have a finite lifespan that necessitates their constant replenishment from self-renewing, multipotent hematopoietic stem cells (HSCs). 1 HSC maintenance and expansion are thought to be regulated by interactions with bone marrow (BM) stromal elements, including osteoblasts 2-4 and vascular endothelial cells, 5 both of which have been proposed to form a supportive HSC "niche." 2,[6][7][8] Osteoblasts, in particular, have been implicated in controlling HSC numbers, and studies in gene-targeted 2 and hormone-treated 6,9 mice show a strong correlation between experimentally induced expansion of osteoblasts and increased HSC frequency. Significantly, most studies of osteoblast function as it relates to HSC have relied on complex in vivo models [10][11][12][13] or on in vitro systems in which osteoblasts are derived ex vivo by extended culture of calvarial precursor cells. 10 Although clearly suggestive, these in vivo analyses are complicated by the unavoidable presence of other, nonosteoblastic cell types, whereas in vitro studies of culture-derived osteoblasts are challenged by the possibility that extended culture may induce changes in osteoblast behavior and/or may fail to properly recapitulate the in vivo conditions under which osteoblasts normally would be formed or regulated. For these reasons, it has been difficult to establish the particular aspects of HSC function that depend on the osteoblastic niche, and this has generated significant controversy regarding the specific role of osteoblasts in HSC regulatio...

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“…Consistent with previous observations demonstrating retinoic acid (RA)-and IFNmediated upregulation of SP100 protein expression in other cell types (Guldner et al, 1992;Pelicano et al, 1997;Yordy et al, 2004), these agents increased the expression of SP100 in endothelial cells (Figure 1a). RA has been shown to both decrease and increase ETS1 protein expression (Raouf et al, 2000;Igarashi et al, 2001), and we observed an increase in ETS1 expression following RA treatment in endothelial cells (Figure 1a).…”

Section: Sp100 and Ets1 Expression Is Induced In Primary Endothelial mentioning

confidence: 64%

SP100 inhibits ETS1 activity in primary endothelial cells

et al. 2004

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The Ets1 proto-oncogene is upregulated by retinoic acid: characterization of a functional retinoic acid response element in the Ets1 promoter

Cited by 31 publications

References 32 publications

The MicroRNA miR-199a-5p Down-regulation Switches on Wound Angiogenesis by Derepressing the v-ets Erythroblastosis Virus E26 Oncogene Homolog 1-Matrix Metalloproteinase-1 Pathway

The MicroRNA miR-199a-5p Down-regulation Switches on Wound Angiogenesis by Derepressing the v-ets Erythroblastosis Virus E26 Oncogene Homolog 1-Matrix Metalloproteinase-1 Pathway

Osteolineage niche cells initiate hematopoietic stem cell mobilization

SP100 inhibits ETS1 activity in primary endothelial cells

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