Sentence examples for migration in endothelial from inspiring English sources

Average RGD spacing similar to that found in fibronectin leads to lipid raft accumulation at FAs, enhances sensitivity to VEGF stimulation, and controls migration in endothelial cells.

We previously found that TSAd regulates VEGFR-2 induced actin polymerisation and migration in endothelial cells [24].

These angiogenic growth factors can increase proliferation, sprouting and migration in endothelial cells [ 5].

VEGF is a key regulator of angiogenesis due to its ability to stimulate proliferation and migration in endothelial cells [ 90 ].

Our current work shows that PC-1 is essential for cell migration in endothelial cells in a process that also likely depends on PI3-kinase.

Conversely, cytokines such as IL-1β and TNF-α stimulate the expression of adhesion molecules required for leukocyte adhesion and migration in endothelial cells [ 13].

Here, we show that suppression of β3-integrin in mice leads to the activation of a neuropilin-1 (NRP1 -dependent cell migratioNRP1 -dependentdothelial cells via a migration that depathwayn NRP1's mobinisation away from maturendothelialesions following VEGF-stimulation.

We investigated the effects of a collection of growth factors potentially involved in the control of proliferation and migration in retinal endothelial cells, the key processes in PDR-associated neovascularization.

Similarly, in cell-based bioassays, VEGF Trap inhibited the activation of VEGFR1 and VEGFR2, as well as VEGF-A induced calcium mobilization and migration in human endothelial cells more potently than ranibizumab or bevacizumab.

Consistent with its higher affinity for VEGF-A and faster association rate, VEGF Trap demonstrates increased potency relative to ranibizumab and bevacizumab in blocking VEGF-A induced activation of VEGFR1 and VEGFR2 in cell-based assays, and also in blocking VEGF-mediated calcium mobilization and migration in human endothelial cells.

Hence, VEGF-A isoform-specific elevation in RCAN1 expression could account for the reduction in VEGF-A-stimulated endothelial cell migration in NFATc2-depleted endothelial cells.