作者: A. Londesborough , K. Vaahtomeri , M. Tiainen , P. Katajisto , N. Ekman
DOI: 10.1242/DEV.017038
关键词:
摘要: Inactivation of the tumor suppressor kinase Lkb1 in mice leads to vascular defects and midgestational lethality at embryonic day 9-11 (E9-E11). Here, we have used conditional targeting investigate underlying Lkb1(-/-) phenotype. Endothelium-restricted deletion led death E12.5 with a loss smooth muscle cells (vSMCs) disruption. Transforming growth factor beta (TGFbeta) pathway activity was reduced Lkb1-deficient endothelial (ECs), TGFbeta signaling from ECs adjacent mesenchyme defective, noted as SMAD2 phosphorylation. The addition mutant yolk sac explants rescued vSMCs, evidenced by alpha actin (SMA) expression. These results reveal an essential function for TGFbeta-mediated vSMC recruitment during angiogenesis.