scholarly journals Azithromycin Attenuates Fibroblast Growth Factors Induced Vascular Endothelial Growth Factor Via p38MAPK Signaling in Human Airway Smooth Muscle Cells

2011 ◽  
Vol 67 (2) ◽  
pp. 331-339 ◽  
Author(s):  
Anna Willems-Widyastuti ◽  
Bart M. Vanaudenaerde ◽  
Robin Vos ◽  
Ellen Dilisen ◽  
Stijn E. Verleden ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Smooth Muscle ◽  
Growth Factors ◽  
Fibroblast Growth Factors ◽  
Airway Smooth Muscle Cells ◽  
Vascular Endothelial ◽  
Fibroblast Growth ◽  
Human Airway Smooth Muscle ◽  
P38mapk Signaling ◽  
Endothelial Growth Factor

Fibroblast growth factor mediates hypoxia-induced endothelin-A receptor expression in lung artery smooth muscle cells

2003 ◽  
Vol 95 (2) ◽  
pp. 643-651 ◽  
Author(s):  
Peng Li ◽  
Suzanne Oparil ◽  
Ju-Zhong Sun ◽  
John A. Thompson ◽  
Yiu-Fai Chen
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Smooth Muscle ◽  
Growth Factors ◽  
Angiotensin Ii ◽  
Growth Factor ◽  
Atrial Natriuretic Peptide ◽  
Tyrosine Kinase Receptor ◽  
Vascular Endothelial ◽  
Fibroblast Growth ◽  
Endothelial Growth Factor

We have previously demonstrated that endothelin (ET)-1 and its subtype A receptor (ET-AR) expression are increased in lung under hypoxic conditions and that activation of ET-AR by ET-1 is a major mediator of hypoxia-induced pulmonary hypertension in the rat. The present study tested the hypothesis that the hypoxia-responsive tyrosine kinase receptor-activating growth factors fibroblast growth factor (FGF)-1, FGF-2, and platelet-derived growth factor (PDGF)-BB stimulate expression of the ET-AR in pulmonary arterial smooth muscle cells (PASMCs). Quiescent rat PASMCs were incubated under hypoxia (1% O2), or with FGF-1, FGF-2, PDGF-BB, vascular endothelial growth factor, ET-1, angiotensin II, or atrial natriuretic peptide under normoxic conditions for 24 h. FGF-1 and -2 and PDGF-BB, but not hypoxia, vascular endothelial growth factor, ET-1, angiotensin II, or atrial natriuretic peptide, significantly increased ET-AR mRNA levels. FGF-1-induced ET-AR expression was inhibited by FGF-receptor inhibitor PD-166866, MEK inhibitor U-0126, transcription inhibitor actinomycin D, and translation inhibitor cycloheximide. In contrast, the stimulatory effect of FGF-1 on ET-AR mRNA expression was not altered by PI3 kinase, PKA, PKC, or adenylate cyclase inhibitors. PASMC ET-AR gene transcription, assessed by nuclear-runoff analysis, was increased by FGF-1. These results provide novel finding that ET-AR in PASMCs in vitro is unresponsive to hypoxia per se but is robustly simulated by tyrosine kinase receptor-associated growth factors (FGF-1, FGF-2, PDGF-BB) that themselves are stimulated by hypoxia in lung. This observation suggests a novel signaling mechanism that may be responsible for overexpression of ET-AR in lung, and may contribute to the hypoxia-induced pulmonary vasoconstriction, hypertension, and vascular remodeling in hypoxia-adapted animal.

scholarly journals Fibroblast Growth Factors and Vascular Endothelial Growth Factor Promote Cardiac Reprogramming under Defined Conditions

2015 ◽  
Vol 5 (6) ◽  
pp. 1128-1142 ◽  
Author(s):  
Hiroyuki Yamakawa ◽  
Naoto Muraoka ◽  
Kazutaka Miyamoto ◽  
Taketaro Sadahiro ◽  
Mari Isomi ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factors ◽  
Growth Factor ◽  
Fibroblast Growth Factors ◽  
Vascular Endothelial ◽  
Fibroblast Growth ◽  
Endothelial Growth Factor

scholarly journals Vasoactive peptides upregulate mRNA expression and secretion of vascular endothelial growth factor in human airway smooth muscle cells

2007 ◽  
Vol 47 (1) ◽  
pp. 109-118 ◽  
Author(s):  
Vijay K. T. Alagappan ◽  
Anna Willems-Widyastuti ◽  
Ann L. B. Seynhaeve ◽  
Ingrid M. Garrelds ◽  
Timo L. M. ten Hagen ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Mrna Expression ◽  
Airway Smooth Muscle Cells ◽  
Vascular Endothelial ◽  
Human Airway Smooth Muscle ◽  
Vasoactive Peptides ◽  
Endothelial Growth Factor
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