| First Author | Jeansson M | Year | 2011 |
| Journal | J Clin Invest | Volume | 121 |
| Issue | 6 | Pages | 2278-89 |
| PubMed ID | 21606590 | Mgi Jnum | J:174022 |
| Mgi Id | MGI:5050788 | Doi | 10.1172/JCI46322 |
| Citation | Jeansson M, et al. (2011) Angiopoietin-1 is essential in mouse vasculature during development and in response to injury. J Clin Invest 121(6):2278-89 |
| abstractText | Angiopoietin-1/Tek signaling is a critical regulator of blood vessel development, with conventional knockout of angiopoietin-1 or Tek in mice being embryonically lethal due to vascular defects. In addition, angiopoietin-1 is thought to be required for the stability of mature vessels. Using a Cre-Lox conditional gene targeting approach, we have studied the role of angiopoietin-1 in embryonic and adult vasculature. We report here that angiopoietin-1 is critical for regulating both the number and diameter of developing vessels but is not required for pericyte recruitment. Cardiac-specific knockout of angiopoietin-1 reproduced the phenotype of the conventional knockout, demonstrating that the early vascular abnormalities arise from flow-dependent defects. Strikingly, deletion in the entire embryo after day E13.5 produced no immediate vascular phenotype. However, when combined with injury or microvascular stress, angiopoietin-1 deficiency resulted in profound organ damage, accelerated angiogenesis, and fibrosis. These findings redefine our understanding of the biological roles of angiopoietin-1: it is dispensable in quiescent vessels but has a powerful ability to modulate the vascular response after injury. |
