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Transforming growth factor-<img src='/image/spc_char/beta.gif' border=0><sub>1</sub> induces angiogenesis <i style="">in vitro</i> via VEGF production in human airway smooth muscle cells

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Title Transforming growth factor-1 induces angiogenesis in vitro via VEGF production in human airway smooth muscle cells
 
Creator Willems-Widyastuti, Anna
Alagappan, Vijay K T
Arulmani, Uday
Vanaudenaerde, Bart M
Boer, Willem I de
Mooi, Wolter J
Verleden, Geert M
Sharma, Hari S
 
Subject Asthma
Chronic obstructive pulmonary diseases (COPD)
Human airway smooth muscle cells (HASMC)
Human umbilical vein endothelial cells (HUVEC)
TGF-1
VEGF
Vascular remodelling
 
Description 262-269
Increase in size and number of bronchial
blood vessels as well as hyperaemia are factors that contribute to airway
wall remodelling in patients with chronic airway diseases, such as asthma and
chronic obstructive pulmonary diseases (COPD). Expression of transforming
growth factor 1
(TGF-1),
a multifunctional cytokine as well as vascular endothelial growth factor
(VEGF), a key angiogenic molecule, has been shown
in the inflammed airways in patients with chronic airway diseases. TGF-1 has been implicated in the
regulation of extracellular matrix, leading to airway remodelling in patients
with chronic airway diseases. However, the role of TGF-1 in regulating VEGF expression in
patients
with chronic airway diseases, as well as the underlying mechanisms are not yet
well established. We investigated whether TGF-1 stimulates VEGF expression in vitro and hence could influence
vascular remodelling. Cultured human airway smooth muscle cells (HASMC) were
serum deprived for 60 h before incubation with 5ng/ml of TGF-1 for different
time points. Control cells received serum-free culture medium. TGF‑1, treatment resulted in time
dependent HASMC
cell proliferation with maximal values for DNA biosynthesis at 24 h and cell
number at 48 h. Northern blot analysis
of VEGF mRNA expression showed increased levels in cells treated with TGF-1 for 4 to 8 h. TGF-1 also induced a
time-dependent release of VEGF proteins in the conditioned medium after 48 h of
treatment. Furthermore, the ability of HASMC-released VEGF proteins to induce
human umbilical vein endothelial cells proliferation was inhibited by VEGF
receptor antagonist, confirming that TGF-1 induced VEGF was biologically
active. We conclude that TGF-1 in addition
to an extracellular matrix regulator also could play a key role in bronchial
angiogenesis and vascular remodelling via
VEGF pathway in asthma.


 
Date 2011-09-16T04:38:38Z
2011-09-16T04:38:38Z
2011-08
 
Type Article
 
Identifier 0975-0959 (Online); 0301-1208 (Print)
http://hdl.handle.net/123456789/12701
 
Language en_US
 
Rights CC Attribution-Noncommercial-No Derivative Works 2.5 India
 
Publisher NISCAIR-CSIR, India
 
Source IJBB Vol.48(4) [August 2011]