scholarly journals Caveolin-1 Down-Regulation Reduces VEGF-A Secretion Induced by IGF-1 in ARPE-19 Cells

Life ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 44
Author(s):  
Alessandra Puddu ◽  
Roberta Sanguineti ◽  
Davide Maggi
Keyword(s):  
Endothelial Cell ◽  
Growth Factor ◽  
Endothelial Cell Migration ◽  
Microvascular Endothelial Cell ◽  
Mrna Levels ◽  
Down Regulation ◽  
Ocular Neovascularization ◽  
Caveolin 1 ◽  
Secretory Products ◽  
Opposite Manner

The insulin-like growth factor 1 (IGF-1) stimulates expression and secretion of vascular endothelial growth factor-A (VEGF-A), the main actor in ocular neovascularization, by RPE cells. Activity of IGF-1 is regulated by interaction between its receptor and Caveolin-1 (Cav-1), the main component of caveolae. The aim of this study was to investigate whether modulation of Cav-1 expression affects synthesis and secretion of VEGF-A. ARPE-19 cells were transfected with small interfering RNA for Cav-1 (si-Cav-1) and with control siRNA (si-CTR) and stimulated with IGF-1. We found that down-regulation of Cav-1 did not affect activation of IGF-1R but regulated in an opposite manner the phosphorylation of Akt and Erk1/2. Moreover, we found that IGF-1 increased mRNA levels of VEGF-A in both si-CTR and in si-Cav-1 ARPE-19 cells and that Cav-1 silencing significantly reduced basal and IGF-1-stimulated VEGF-A release. Then we investigated the response of the microvascular endothelial cell line HMEC-1 to secretory products of ARPE-19 cells by evaluating wound healing closure, finding that conditioned media from si-Cav-1-ARPE-19 cells reduced endothelial cell migration rate. These data demonstrate that Cav-1 regulates secretion of VEGF-A, and that the depletion of Cav-1 reduces IGF-1 induced VEGF-A secretion in ARPE-19 cells and the migratory potential of their secretory products.

Inhibition of endothelial cell migration and angiogenesis by a vascular endothelial growth factor receptor-1 derived peptide

2008 ◽  
Vol 44 (13) ◽  
pp. 1914-1921 ◽  
Author(s):  
Pedro M. Lacal ◽  
Veronica Morea ◽  
Federica Ruffini ◽  
Angela Orecchia ◽  
Annalisa S. Dorio ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Endothelial Cell Migration ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Caveolin-1 orchestrates fibroblast growth factor 2 signaling control of angiogenesis in placental artery endothelial cell caveolae

2012 ◽  
Vol 227 (6) ◽  
pp. 2480-2491 ◽  
Author(s):  
Lin Feng ◽  
Wu-Xiang Liao ◽  
Quan Luo ◽  
Hong-Hai Zhang ◽  
Wen Wang ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Caveolin 1

scholarly journals A Central Role for Nicotinic Cholinergic Regulation of Growth Factor–Induced Endothelial Cell Migration

2007 ◽  
Vol 27 (1) ◽  
pp. 106-112 ◽  
Author(s):  
Martin K.C. Ng ◽  
Jenny Wu ◽  
Edwin Chang ◽  
Bing-yin Wang ◽  
Regina Katzenberg-Clark ◽  
...  
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Endothelial Cell Migration ◽  
Cholinergic Regulation ◽  
Regulation Of Growth

scholarly journals Monocyte activation state regulates monocyte-induced endothelial proliferation through Met signaling

Blood ◽  
2010 ◽  
Vol 115 (16) ◽  
pp. 3407-3412 ◽  
Author(s):  
Shai Y. Schubert ◽  
Alejandro Benarroch ◽  
Juan Monter-Solans ◽  
Elazer R. Edelman
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Direct Interaction ◽  
Endothelial Cell Proliferation ◽  
Specific Cell ◽  
Mrna Levels ◽  
Hepatocyte Growth

Abstract Direct interaction of unactivated primary monocytes with endothelial cells induces a mitogenic effect in subconfluent, injured endothelial monolayers through activation of endothelial Met. We now report that monocytes' contact-dependent mitogenicity is controlled by activation-mediated regulation of hepatocyte growth factor. Direct interaction of unactivated monocytes with subconfluent endothelial cells for 12 hours resulted in 9- and 120-fold increase in monocyte tumor necrosis factor-α (TNFα) and interleukin-1β (IL-1β) mRNA levels and bitemporal spike in hepatocyte growth factor that closely correlates with endothelial Met and extracellular signal-related kinase (ERK) phosphorylation. Once activated, monocytes cannot induce a second wave of endothelial cell proliferation and endothelial Met phosphorylation and soluble hepatocyte growth factor levels fall off. Monocyte-induced proliferation is dose dependent and limited to the induction of a single cell cycle. Monocytes retain their ability to activate other endothelial cells for up to 8 hours after initial interaction, after which they are committed to the specific cell. There is therefore a profoundly sophisticated mode of vascular repair. Confluent endothelial cells ensure vascular quiescence, whereas subconfluence promotes vessel activation. Simultaneously, circulating monocytes stimulate endothelial cell proliferation, but lose this potential once activated. Such a system provides for the fine balance that can restore vascular and endothelial homeostasis with minimal overcompensation.

scholarly journals Redox Regulation of SERCA2 Is Required for Vascular Endothelial Growth Factor-Induced Signaling and Endothelial Cell Migration

2012 ◽  
Vol 17 (8) ◽  
pp. 1099-1108 ◽  
Author(s):  
Alicia M. Evangelista ◽  
Melissa D. Thompson ◽  
Robert M. Weisbrod ◽  
David R. Pimental ◽  
XiaoYong Tong ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Redox Regulation ◽  
Endothelial Cell Migration ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor
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