VE‐cadherin‐CreER<sup>T2</sup> transgenic mouse: A model for inducible recombination in the endothelium

Monvoisin, Arnaud; Alva, Jackelyn A.; Hofmann, Jennifer; Zovein, Ann C.; Lane, Timothy F.; Iruela‐Arispe, M. Luisa

doi:10.1002/dvdy.20982

Cited by 224 publications

(228 citation statements)

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“…To determine a functional relevance of Wt1 for tumour vessel formation and tumorigenesis, we used Wt1 conditional knockout mice (Wt1 lox/lox ) 17 crossed either with a tamoxifen-inducible Tie2-Cre 18 or VE-cadherin-Cre 19 (Supplementary Table 1). Both of them have been described to be active in endothelial cells.…”

Section: Resultsmentioning

confidence: 99%

“…We confirmed the high contribution of Wt1-expressing cells to the tumour stroma in mice. To determine the relevance of Wt1 for tumour vessel formation and cancer progression, and to distinguish between the effects of a purely endothelial-specific and a broader Wt1 knockout, affecting other stromal cell types, we used Wt1 conditional knockout mice (Wt1 lox/lox ) 17 crossed either with a tamoxifen-inducible VE-cadherin-Cre 19 or a Tie2-Cre 18 . Both Cre lines are active in endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…VE-cadherin-CreERT2 (ref. 19) mice obtained from L. IruelaArispe were crossed with Wt1 lox/lox animals to generate the VE-CreERT2;Wt1 lox/lox strain. Both Cre lines were backcrossed four times with C57BL6.…”

Section: Methodsmentioning

confidence: 99%

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The Wilms’ tumour suppressor Wt1 is a major regulator of tumour angiogenesis and progression

et al. 2014

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Angiogenesis, activation of metastasis and avoidance of immune destruction are important for cancer progression. These biological capabilities are, apart from cancer cells, mediated by different cell types, including endothelial, haematopoietic progenitor and myeloid-derived suppressor cells. We show here that all these cell types frequently express the Wilms' tumour suppressor Wt1, which transcriptionally controls expression of Pecam-1 (CD31) and c-kit (CD117). Inducible conditional knockout of Wt1 in endothelial, haematopoietic and myeloidderived suppressor cells is sufficient to cause regression of tumour vascularization and an enhanced immune response, leading to decreased metastasis, regression of established tumours and enhanced survival. Thus, Wt1 is an important regulator of cancer growth via modulation of tumour vascularization, immune response and metastasis formation.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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The Wilms’ tumour suppressor Wt1 is a major regulator of tumour angiogenesis and progression

et al. 2014

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“…This may reflect differences in the efficiency of Cre transgenics 38,39 and of conditional Itgb1 strains 16,40 . The whole open reading frame of the Itgb1 gene is flanked by loxP sites in the line employed for most of the experiments by Zovein et al 15 and, as was shown by the same group, integrin b1 protein expression in this mouse strain can persist from a circular DNA fragment even after Cre recombination 41 .…”

Section: Discussionmentioning

confidence: 99%

Integrin β1 controls VE-cadherin localization and blood vessel stability

et al. 2015

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Angiogenic blood vessel growth requires several distinct but integrated cellular activities. Endothelial cell sprouting and proliferation lead to the expansion of the vasculature and give rise to a highly branched, immature plexus, which is subsequently reorganized into a mature and stable network. Although it is known that integrin-mediated cell-matrix interactions are indispensable for embryonic angiogenesis, little is known about the function of integrins in different steps of vascular morphogenesis. Here, by investigating the integrin b1-subunit with inducible and endothelial-specific gene targeting in the postnatal mouse retina, we show that b1 integrin promotes endothelial sprouting but is a negative regulator of proliferation. In maturing vessels, integrin b1 is indispensable for proper localization of VE-cadherin and thereby cell-cell junction integrity. The sum of our findings establishes that integrin b1 has critical functions in the growing and maturing vasculature, and is required for the formation of stable, non-leaky blood vessels.

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“…They generated mice with tamoxifen-inducible and endothelium-selective Neuregulin1 gene knockout by cross-breeding mice with VE-cadherin promoter driven Cre-ER (Monvoisin et al, 2006) and mice carrying homozygously floxed alleles of the Neuregulin1 gene (Yang et al, 2001). At the baseline, hearts from these knockout mice showed normal wall thickness, left ventricular chamber size, and systolic function.…”

Section: Transgenic Mouse Models With Mutations Of the Neuregulin1 Genementioning

confidence: 99%

Neuregulin1-ErbB Signaling in Doxorubicin-Induced Cardiotoxicity

Goukassian¹,

Morgan²,

Yan³

2012

Cardiotoxicity of Oncologic Treatments

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VE‐cadherin‐CreER^T2 transgenic mouse: A model for inducible recombination in the endothelium

Cited by 224 publications

References 24 publications

The Wilms’ tumour suppressor Wt1 is a major regulator of tumour angiogenesis and progression

The Wilms’ tumour suppressor Wt1 is a major regulator of tumour angiogenesis and progression

Integrin β1 controls VE-cadherin localization and blood vessel stability

Neuregulin1-ErbB Signaling in Doxorubicin-Induced Cardiotoxicity

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VE‐cadherin‐CreERT2 transgenic mouse: A model for inducible recombination in the endothelium

Cited by 224 publications

References 24 publications

The Wilms’ tumour suppressor Wt1 is a major regulator of tumour angiogenesis and progression

The Wilms’ tumour suppressor Wt1 is a major regulator of tumour angiogenesis and progression

Integrin β1 controls VE-cadherin localization and blood vessel stability

Neuregulin1-ErbB Signaling in Doxorubicin-Induced Cardiotoxicity

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Product

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VE‐cadherin‐CreER^T2 transgenic mouse: A model for inducible recombination in the endothelium