| First Author | Takimoto A | Year | 2009 |
| Journal | Dev Biol | Volume | 332 |
| Issue | 2 | Pages | 196-211 |
| PubMed ID | 19464280 | Mgi Jnum | J:152868 |
| Mgi Id | MGI:4360157 | Doi | 10.1016/j.ydbio.2009.05.552 |
| Citation | Takimoto A, et al. (2009) Differential actions of VEGF-A isoforms on perichondrial angiogenesis during endochondral bone formation. Dev Biol 332(2):196-211 |
| abstractText | During endochondral bone formation, vascular invasion initiates the replacement of avascular cartilage by bone. We demonstrate herein that the cartilage-specific overexpression of VEGF-A(164) in mice results in the hypervascularization of soft connective tissues away from cartilage. Unexpectedly, perichondrial tissue remained avascular in addition to cartilage. Hypervascularization of tissues similarly occurred when various VEGF-A isoforms were overexpressed in the chick forelimb, but also in this case perichondrial tissue and cartilage were completely devoid of vasculature. However, following bony collar formation, anti-angiogenic properties in perichondrial tissue were lost and perichondrial angiogenesis was accelerated by VEGF-A(146), VEGF-A(166), or VEGF-A(190). Once the perichondrium was vascularized, osteoclast precursors were recruited from the circulation and the induction of MMP9 and MMP13 can be observed in parallel with the activation of TGF-beta signaling. Neither perichondrial angiogenesis nor the subsequent cartilage vascularization was found to be accelerated by the non-heparin-binding VEGF-A(122) or by the VEGF-A(166)DeltaE(162)-R(166) mutant lacking a neuropilin-binding motif. Hence, perichondrial angiogenesis is a prerequisite for subsequent cartilage vascularization and is differentially regulated by VEGF-A isoforms. |
