Id1 restrains p21 expression to control endothelial progenitor cell formation

Research output: Contribution to journalArticle

Alessia Ciarrocchi, Vladimir Jankovic, Yuval Shaked, Daniel J. Nolan, Vivek Mittal, Robert S. Kerbel, Stephen D. Nimer, Robert Benezra

Loss of Id1 in the bone marrow (BM) severely impairs tumor angiogenesis resulting in significant inhibition of tumor growth. This phenotype has been associated with the absence of circulating endothelial progenitor cells (EPCs) in the peripheral of Id1 mutant mice. However, the manner in which Id1 loss in the BM controls EPC generation or mobilization is largely unknown. Using genetically modified mouse models we demonstrate here that the generation of EPCs in the BM depends the ability of Id1 to restrain the expression of its target gene p21. Through a series of cellular and functional studies we that the increased myeloid commitment of BM stem cells and the absence of EPCs in Id1 knockout mice are associated elevated p21 expression. Genetic ablation of p21 rescues the EPC population in the Id1 null animals, re-establishing functional BM-derived angiogenesis and restoring normal tumor growth. These results demonstrate that the restraint of p21 expression by Id1 is one key element of its activity in facilitating the generation of EPCs in the BM and highlight the critical role these play in tumor angiogenesis.

Original languageEnglish
Article numbere1338
JournalPLoS ONE
Volume2
Issue number12
DOIs
StatePublished - Dec 19 2007

PMID: 18092003

PMCID: PMC2129121

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Id1 restrains p21 expression to control endothelial progenitor cell formation. / Ciarrocchi, Alessia; Jankovic, Vladimir; Shaked, Yuval; Nolan, Daniel J.; Mittal, Vivek; Kerbel, Robert S.; Nimer, Stephen D.; Benezra, Robert.

In: PLoS ONE, Vol. 2, No. 12, e1338, 19.12.2007.

Research output: Contribution to journalArticle

Harvard

Ciarrocchi, A, Jankovic, V, Shaked, Y, Nolan, DJ, Mittal, V, Kerbel, RS, Nimer, SD & Benezra, R 2007, 'Id1 restrains p21 expression to control endothelial progenitor cell formation' PLoS ONE, vol. 2, no. 12, e1338. https://doi.org/10.1371/journal.pone.0001338

APA

Ciarrocchi, A., Jankovic, V., Shaked, Y., Nolan, D. J., Mittal, V., Kerbel, R. S., ... Benezra, R. (2007). Id1 restrains p21 expression to control endothelial progenitor cell formation. PLoS ONE, 2(12), [e1338]. https://doi.org/10.1371/journal.pone.0001338

Vancouver

Ciarrocchi A, Jankovic V, Shaked Y, Nolan DJ, Mittal V, Kerbel RS et al. Id1 restrains p21 expression to control endothelial progenitor cell formation. PLoS ONE. 2007 Dec 19;2(12). e1338. https://doi.org/10.1371/journal.pone.0001338

Author

Ciarrocchi, Alessia ; Jankovic, Vladimir ; Shaked, Yuval ; Nolan, Daniel J. ; Mittal, Vivek ; Kerbel, Robert S. ; Nimer, Stephen D. ; Benezra, Robert. / Id1 restrains p21 expression to control endothelial progenitor cell formation. In: PLoS ONE. 2007 ; Vol. 2, No. 12.

BibTeX

@article{ddba0ed1880046148dd2e6a39bbdf144,
title = "Id1 restrains p21 expression to control endothelial progenitor cell formation",
abstract = "Loss of Id1 in the bone marrow (BM) severely impairs tumor angiogenesis resulting in significant inhibition of tumor growth. This phenotype has been associated with the absence of circulating endothelial progenitor cells (EPCs) in the peripheral of Id1 mutant mice. However, the manner in which Id1 loss in the BM controls EPC generation or mobilization is largely unknown. Using genetically modified mouse models we demonstrate here that the generation of EPCs in the BM depends the ability of Id1 to restrain the expression of its target gene p21. Through a series of cellular and functional studies we that the increased myeloid commitment of BM stem cells and the absence of EPCs in Id1 knockout mice are associated elevated p21 expression. Genetic ablation of p21 rescues the EPC population in the Id1 null animals, re-establishing functional BM-derived angiogenesis and restoring normal tumor growth. These results demonstrate that the restraint of p21 expression by Id1 is one key element of its activity in facilitating the generation of EPCs in the BM and highlight the critical role these play in tumor angiogenesis.",
author = "Alessia Ciarrocchi and Vladimir Jankovic and Yuval Shaked and Nolan, {Daniel J.} and Vivek Mittal and Kerbel, {Robert S.} and Nimer, {Stephen D.} and Robert Benezra",
year = "2007",
month = "12",
day = "19",
doi = "10.1371/journal.pone.0001338",
language = "English",
volume = "2",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "12",

}

RIS

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T1 - Id1 restrains p21 expression to control endothelial progenitor cell formation

AU - Ciarrocchi, Alessia

AU - Jankovic, Vladimir

AU - Shaked, Yuval

AU - Nolan, Daniel J.

AU - Mittal, Vivek

AU - Kerbel, Robert S.

AU - Nimer, Stephen D.

AU - Benezra, Robert

PY - 2007/12/19

Y1 - 2007/12/19

N2 - Loss of Id1 in the bone marrow (BM) severely impairs tumor angiogenesis resulting in significant inhibition of tumor growth. This phenotype has been associated with the absence of circulating endothelial progenitor cells (EPCs) in the peripheral of Id1 mutant mice. However, the manner in which Id1 loss in the BM controls EPC generation or mobilization is largely unknown. Using genetically modified mouse models we demonstrate here that the generation of EPCs in the BM depends the ability of Id1 to restrain the expression of its target gene p21. Through a series of cellular and functional studies we that the increased myeloid commitment of BM stem cells and the absence of EPCs in Id1 knockout mice are associated elevated p21 expression. Genetic ablation of p21 rescues the EPC population in the Id1 null animals, re-establishing functional BM-derived angiogenesis and restoring normal tumor growth. These results demonstrate that the restraint of p21 expression by Id1 is one key element of its activity in facilitating the generation of EPCs in the BM and highlight the critical role these play in tumor angiogenesis.

AB - Loss of Id1 in the bone marrow (BM) severely impairs tumor angiogenesis resulting in significant inhibition of tumor growth. This phenotype has been associated with the absence of circulating endothelial progenitor cells (EPCs) in the peripheral of Id1 mutant mice. However, the manner in which Id1 loss in the BM controls EPC generation or mobilization is largely unknown. Using genetically modified mouse models we demonstrate here that the generation of EPCs in the BM depends the ability of Id1 to restrain the expression of its target gene p21. Through a series of cellular and functional studies we that the increased myeloid commitment of BM stem cells and the absence of EPCs in Id1 knockout mice are associated elevated p21 expression. Genetic ablation of p21 rescues the EPC population in the Id1 null animals, re-establishing functional BM-derived angiogenesis and restoring normal tumor growth. These results demonstrate that the restraint of p21 expression by Id1 is one key element of its activity in facilitating the generation of EPCs in the BM and highlight the critical role these play in tumor angiogenesis.

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U2 - 10.1371/journal.pone.0001338

DO - 10.1371/journal.pone.0001338

M3 - Article

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JO - PLoS ONE

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JF - PLoS ONE

SN - 1932-6203

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M1 - e1338

ER -

ID: 3340474