Proprotein convertase furin enhances survival and migration of vascular smooth muscle cells via processing of pro-nerve growth factor

2012 ◽  
Vol 153 (2) ◽  
pp. 197-207 ◽  
Author(s):  
D. Urban ◽  
J. Lorenz ◽  
H. Meyborg ◽  
S. Ghosh ◽  
U. Kintscher ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Proprotein Convertase ◽  
Nerve Growth ◽  
And Migration

Nerve growth factor synthesis in human vascular smooth muscle cells and its regulation by dexamethasone

2009 ◽  
Vol 157 (1-3) ◽  
pp. 3-7 ◽  
Author(s):  
Christoph Schäper ◽  
Sven Gläser ◽  
David A. Groneberg ◽  
Gert Kunkel ◽  
Ralf Ewert ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Nerve Growth ◽  
Nerve Growth Factor Synthesis

scholarly journals Sortilin Expression Is Essential for Pro-Nerve Growth Factor-Induced Apoptosis of Rat Vascular Smooth Muscle Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e84969 ◽  
Author(s):  
Luisa Campagnolo ◽  
Gaetana Costanza ◽  
Arianna Francesconi ◽  
Gaetano Arcuri ◽  
Ilana Moscatelli ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Nerve Growth ◽  
Induced Apoptosis

Signal transduction of betacellulin in growth and migration of vascular smooth muscle cells

2004 ◽  
Vol 287 (3) ◽  
pp. C807-C813 ◽  
Author(s):  
Mizuo Mifune ◽  
Haruhiko Ohtsu ◽  
Hiroyuki Suzuki ◽  
Gerald D. Frank ◽  
Tadashi Inagami ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Remodeling ◽  
Muscle Cells ◽  
Egf Family ◽  
And Migration

Epidermal growth factor (EGF) family ligands have been implicated in cardiovascular diseases because of their enhanced expression in vascular lesions and their promoting effects on growth and migration of vascular smooth muscle cells (VSMCs). Betacellulin (BTC), a novel EGF family ligand, has been shown to be expressed in atherosclerotic lesions and to be a potent growth factor of VSMCs. However, the molecular mechanisms downstream of BTC involved in mediating vascular remodeling remain largely unknown. Therefore, the aim of this study was to examine the effects of BTC on signal transduction, growth, and migration in VSMCs. We found that BTC stimulated phosphorylation of EGF receptor (EGFR) at Tyr1068, which was completely blocked by an EGFR kinase inhibitor, AG-1478. BTC also phosphorylated ErbB2 at Tyr877, Tyr1112, and Tyr1248 and induced association of ErbB2 with EGFR, suggesting their heterodimerization in VSMCs. In postreceptor signal transduction, BTC stimulated phosphorylation of extracellular signal-regulated kinase (ERK)1/2, Akt, and p38 mitogen-activated protein kinase (MAPK). Moreover, BTC stimulated proliferation and migration of VSMCs. ERK and Akt inhibitors suppressed migration markedly and proliferation partially, whereas the p38 inhibitor suppressed migration partially but not proliferation. In addition, we found the presence of endogenous BTC in conditioned medium of VSMCs and an increase of BTC on angiotensin II stimulation. In summary, BTC promotes growth and migration of VSMCs through activation of EGFR, ErbB2, and downstream serine/threonine kinases. Together with the expression and processing of endogenous BTC in VSMCs, our results suggest a critical involvement of BTC in vascular remodeling.

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