作者: S. Majka , K. Fox , B. McGuire , J. Crossno , P. McGuire
DOI: 10.1152/AJPLUNG.00175.2005
关键词: Lung morphogenesis 、 Autocrine signalling 、 Cell biology 、 Paracrine signalling 、 Receptor 、 Cell 、 Biology 、 Cell cycle 、 Contact inhibition 、 Mesenchymal stem cell
摘要: Tight regulation of VEGF-A production and signaling is important for the maintenance lung development homeostasis. VEGF null mice have provided little insight into role during later stages morphogenesis. Therefore, we examined in vitro effects autocrine paracrine inhibition on a Flk-1-negative subset fetal pulmonary mesenchymal cells (pMC). We hypothesized that receptor regulates turnover mesenchyme cell cycle-dependent manner. blockade with SU-5416 caused spreading decreased proliferation bcl-2 localization. Nuclear expression cycle inhibitory protein, p21, was increased treatment, p27 absent. Autocrine by pMC resulted p21/p27-dependent contact inhibition. In contrast, exogenous progression through cycle. Selective activation Flt placental growth factor demonstrated importance this receptor/kinase responsiveness pMC. The localization survival dependent VEGF. These results provide evidence plays critical proliferation, survival, subsequent normal architecture control.