| First Author | Turner CJ | Year | 2015 |
| Journal | Development | Volume | 142 |
| Issue | 4 | Pages | 797-808 |
| PubMed ID | 25670798 | Mgi Jnum | J:218158 |
| Mgi Id | MGI:5616934 | Doi | 10.1242/dev.117572 |
| Citation | Turner CJ, et al. (2015) alpha5 and alphav integrins cooperate to regulate vascular smooth muscle and neural crest functions in vivo. Development 142(4):797-808 |
| abstractText | The RGD-binding alpha5 and alphav integrins have been shown to be key regulators of vascular smooth muscle cell (vSMC) function in vitro. However, their role on vSMCs during vascular development in vivo remains unclear. To address this issue, we have generated mice that lack alpha5, alphav or both alpha5 and alphav integrins on their vSMCs, using the SM22alpha-Cre transgenic mouse line. To our surprise, neither alpha5 nor alphav mutants displayed any obvious vascular defects during embryonic development. By contrast, mice lacking both alpha5 and alphav integrins developed interrupted aortic arches, large brachiocephalic/carotid artery aneurysms and cardiac septation defects, but developed extensive and apparently normal vasculature in the skin. Cardiovascular defects were also found, along with cleft palates and ectopically located thymi, in Wnt1-Cre alpha5/alphav mutants, suggesting that alpha5 and alphav cooperate on neural crest-derived cells to control the remodelling of the pharyngeal arches and the septation of the heart and outflow tract. Analysis of cultured alpha5/alphav-deficient vSMCs suggests that this is achieved, at least in part, through proper assembly of RGD-containing extracellular matrix proteins and the correct incorporation and activation of latent TGF-beta. |
