References of "Struman, Ingrid"
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See detailAspects moléculaires du cancer du sein triple négatif et les implications thérapeutiques
COLLIGNON, Joëlle ULg; Struman, Ingrid ULg; Tabruyn, Sébastien ULg et al

in Revue Médicale de Liège (2011), 66(5-6), 393-396

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See detailMicroRNA-21 Exhibits Antiangiogenic Function by Targeting RhoB Expression in Endothelial Cells.
Sabatel, Céline; Malvaux, Ludovic ULg; Bovy, Nicolas ULg et al

in PLoS ONE (2011), 6(2), 16979

BACKGROUND: MicroRNAs (miRNAs) are endogenously expressed small non-coding RNAs that regulate gene expression at post-transcriptional level. The recent discovery of the involvement of these RNAs in the ... [more ▼]

BACKGROUND: MicroRNAs (miRNAs) are endogenously expressed small non-coding RNAs that regulate gene expression at post-transcriptional level. The recent discovery of the involvement of these RNAs in the control of angiogenesis renders them very attractive in the development of new approaches for restoring the angiogenic balance. Whereas miRNA-21 has been demonstrated to be highly expressed in endothelial cells, the potential function of this miRNA in angiogenesis has never been investigated. METHODOLOGY/PRINCIPAL FINDINGS: We first observed in endothelial cells a negative regulation of miR-21 expression by serum and bFGF, two pro-angiogenic factors. Then using in vitro angiogenic assays, we observed that miR-21 acts as a negative modulator of angiogenesis. miR-21 overexpression reduced endothelial cell proliferation, migration and the ability of these cells to form tubes whereas miR-21 inhibition using a LNA-anti-miR led to opposite effects. Expression of miR-21 in endothelial cells also led to a reduction in the organization of actin into stress fibers, which may explain the decrease in cell migration. Further mechanistic studies showed that miR-21 targets RhoB, as revealed by a decrease in RhoB expression and activity in miR-21 overexpressing cells. RhoB silencing impairs endothelial cell migration and tubulogenesis, thus providing a possible mechanism for miR-21 to inhibit angiogenesis. Finally, the therapeutic potential of miR-21 as an angiogenesis inhibitor was demonstrated in vivo in a mouse model of choroidal neovascularization. CONCLUSIONS/SIGNIFICANCE: Our results identify miR-21 as a new angiogenesis inhibitor and suggest that inhibition of cell migration and tubulogenesis is mediated through repression of RhoB. [less ▲]

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See detailMir-146a : A new angiostatic miRNA with tumor-suppressive properties
Halkein, Julie ULg; Castermans, Karolien; Malvaux, Ludovic et al

Poster (2010, October)

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See detailInvolvement of miR-125b in in vitro and in vivo angiogenesis
Malvaux, Ludovic; Pendeville, Hélène; Sabatel, Céline et al

Poster (2010, May 21)

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See detailmiR-146a: an anti-angiogenic miRNA regulated by NF-kB
Halkein, Julie ULg; Tabruyn, Sébastien ULg; Malvaux, Ludovic et al

Poster (2010, May 21)

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See detail16K human prolactin is an anti-lymphangiogenic factor in vitro and in vivo
Kinet, Virginie; Castermans, Karolien; Blacher, Silvia ULg et al

Poster (2010, May 21)

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See detailStudy of the role of miR-21 in the regulation of angiogenesis
Sabatel, Céline; Malvaux, Ludovic; Bovy, Nicolas ULg et al

Poster (2010, May)

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See detailStudy of the role of miR-21 in the regulation of angiogenesis
Sabatel, Céline; Malvaux, Ludovic; Bovy, Nicolas ULg et al

Poster (2010, March)

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See detailInvolvement of miR-125b in in vitro and in vivo angiogenesis
Malvaux, Ludovic; Pendeville, Hélène; Sabatel, Céline et al

Poster (2010, March)

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See detail16K human prolactin is an anti-lymphangiogenic factor in vitro and in vivo
Kinet, Virginie; Castermans, Karolien; Blacher, Silvia ULg et al

Poster (2010, March)

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See detailEvaluation of bromocriptine in the treatment of acute severe peripartum cardiomyopathy: a proof-of-concept pilot study.
Sliwa, Karen; Blauwet, Lori; Tibazarwa, Kemi et al

in Circulation (2010), 121(13), 1465-73

BACKGROUND: Peripartum cardiomyopathy (PPCM) is a potentially life-threatening heart disease that occurs in previously healthy women. We identified prolactin, mainly its 16-kDa angiostatic and ... [more ▼]

BACKGROUND: Peripartum cardiomyopathy (PPCM) is a potentially life-threatening heart disease that occurs in previously healthy women. We identified prolactin, mainly its 16-kDa angiostatic and proapoptotic form, as a key factor in PPCM pathophysiology. Previous reports suggest that bromocriptine may have beneficial effects in women with acute onset of PPCM. METHODS AND RESULTS: A prospective, single-center, randomized, open-label, proof-of-concept pilot study of women with newly diagnosed PPCM receiving standard care (PPCM-Std; n=10) versus standard care plus bromocriptine for 8 weeks (PPCM-Br, n=10) was conducted. Because mothers receiving bromocriptine could not breast-feed, the 6-month outcome of their children (n=21) was studied as a secondary end point. Blinded clinical, hemodynamic, and echocardiographic assessments were performed at baseline and 6 months after diagnosis. Cardiac magnetic resonance imaging was performed 4 to 6 weeks after diagnosis in PPCM-Br patients. There were no significant differences in baseline characteristics, including serum 16-kDa prolactin levels and cathepsin D activity, between the 2 study groups. PPCM-Br patients displayed greater recovery of left ventricular ejection fraction (27% to 58%; P=0.012) compared with PPCM-Std patients (27% to 36%) at 6 months. One patient in the PPCM-Br group died compared with 4 patients in the PPCM-Std group. Significantly fewer PPCM-Br patients (n=1, 10%) experienced the composite end point of poor outcome defined as death, New York Heart Association functional class III/IV, or left ventricular ejection fraction <35% at 6 months compared with the PPCM-Std patients (n=8, 80%; P=0.006). Cardiac magnetic resonance imaging revealed no intracavitary thrombi. Infants of mothers in both groups showed normal growth and survival. CONCLUSIONS: In this trial, the addition of bromocriptine to standard heart failure therapy appeared to improve left ventricular ejection fraction and a composite clinical outcome in women with acute severe PPCM, although the number of patients studied was small and the results cannot be considered definitive. Larger-scale multicenter and blinded studies are in progress to test this strategy more robustly. [less ▲]

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See detailSprouty1, a new target of the angiostatic agent 16K prolactin, negatively regulates angiogenesis
Sabatel, Céline ULg; Cornet, Anne ULg; Tabruyn, Sébastien ULg et al

in Molecular Cancer (2010), 9(1), 231

BACKGROUND:Disorganized angiogenesis is associated with several pathologies, including cancer. The identification of new genes that control tumor neovascularization can provide novel insights for future ... [more ▼]

BACKGROUND:Disorganized angiogenesis is associated with several pathologies, including cancer. The identification of new genes that control tumor neovascularization can provide novel insights for future anti-cancer therapies. Sprouty1 (SPRY1), an inhibitor of the MAPK pathway, might be one of these new genes. We identified SPRY1 by comparing the transcriptomes of untreated endothelial cells with those of endothelial cells treated by the angiostatic agent 16K prolactin (16K hPRL). In the present study, we aimed to explore the potential function of SPRY1 in angiogenesis.RESULTS:We confirmed 16K hPRL induced up-regulation of SPRY1 in primary endothelial cells. In addition, we demonstrated the positive SPRY1 regulation in a chimeric mouse model of human colon carcinoma in which 16K hPRL treatment was shown to delay tumor growth. Expression profiling by qRT-PCR with species-specific primers revealed that induction of SPRY1 expression by 16K hPRL occurs only in the (murine) endothelial compartment and not in the (human) tumor compartment. The regulation of SPRY1 expression was NF-kappaB dependent. Partial SPRY1 knockdown by RNA interference protected endothelial cells from apoptosis as well as increased endothelial cell proliferation, migration, capillary network formation, and adhesion to extracellular matrix proteins. SPRY1 knockdown was also shown to affect the expression of cyclinD1 and p21 both involved in cell-cycle regulation. These findings are discussed in relation to the role of SPRY1 as an inhibitor of ERK/MAPK signaling and to a possible explanation of its effect on cell proliferation.CONCLUSIONS:Taken together, these results suggest that SPRY1 is an endogenous angiogenesis inhibitor. [less ▲]

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See detailFinding miRNAs able to regulate angiogenesis
Pendeville, Helene; Nivelles, Olivier ULg; Malvaux, L. et al

Poster (2009, July)

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See detailFinding Mir able to regulate angiogenesis
Pendeville, Helene; Nivelles, Olivier ULg; Malvaux, L. et al

Poster (2009, May 29)

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See detailStudy of the role of microRNAs in angiogenesis
Malvaux, Ludovic; Pendeville, Hélène; Sabatel, Céline et al

Poster (2009, May 29)

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See detailStudy of the potential regulation of Sprouty1, an angiogenesis inhibitor, by miR-21
Sabatel, Céline; Malvaux, Ludovic; Cornet, Anne et al

Poster (2009, May 29)

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See detailEvaluation of the antitumor activity of 16K prolactin
Kinet, Virginie; Nguyen, Ngoc-Quynh-Nhu ULg; Sabatel, Céline et al

Poster (2009)

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See detailRegulation of microRNAs expression by the antiangiogenic factor 16K hPRL
Halkein, Julie ULg; Malvaux, Ludovic; Nguyen, Ngoc-Quynh-Nhu ULg et al

Poster (2009)

Detailed reference viewed: 13 (0 ULg)