p130Rb2 and p27kip1 cooperate to control mobilization of angiogenic progenitors from the bone marrow

Anxo Vidal, Stergios Zacharoulis, Wenjun Guo, David Shaffer, Filippo Giancotti, Anna H. Bramley, Carmen De La Hoz, Kristian K. Jensen, Daniel Kato, Daniel D. MacDonald, Joseph Knowles, Nancy Yeh, Lawrence A. Frohman, Shahin Rafii, David Lyden, Andrew Koff

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


Neoangiogenesis involves both bone marrow-derived myelomonocytic and endothelial progenitor cells as well as endothelial cells coopted from surrounding vessels. Cytokines induce these cells to proliferate, migrate, and exit the cell cycle to establish the vasculature; however, which cell cycle regulators play a role in these processes is largely unknown. Here, we report that mice lacking the cell cycle inhibitors p130 and p27 show defects in tumor neoangiogenesis, both in xenografts and spontaneously arising tumors. This defect is associated with impaired mobilization of endothelial and myelomonocytic angiogenic progenitors from the bone marrow. This article documents the role of these molecules in angiogenesis and further suggests that cell expansion and mobilization from the bone marrow of angiogenic precursors are separable events.

Original languageEnglish (US)
Pages (from-to)6890-6895
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number19
StatePublished - May 10 2005
Externally publishedYes


  • Angiogenesis
  • Cyclin-dependent kinase inhibitors
  • Stem cell

ASJC Scopus subject areas

  • General


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