Please use this identifier to cite or link to this item: http://nopr.niscair.res.in/handle/123456789/12701
Title: 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
Authors: 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
Keywords: Asthma
Chronic obstructive pulmonary diseases (COPD)
Human airway smooth muscle cells (HASMC)
Human umbilical vein endothelial cells (HUVEC)
TGF-<img src='/image/spc_char/beta.gif' border=0>1
VEGF
Vascular remodelling
Issue Date: Aug-2011
Publisher: NISCAIR-CSIR, India
Abstract: 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 <img src='/image/spc_char/beta.gif' border=0><sub>1</sub> (TGF-<img src='/image/spc_char/beta.gif' border=0><sub>1</sub>), a multifunctional cytokine as well as vascular endothelial growth factor (VEGF), a key angiogenic molecule<span style="color: rgb(204, 0, 153);">, has been shown in the inflammed airways in patients with chronic airway diseases. TGF-<img src='/image/spc_char/beta.gif' border=0><sub>1</sub> has been implicated in the regulation of extracellular matrix, leading to airway remodelling in patients with chronic airway diseases. However, the role of TGF-<img src='/image/spc_char/beta.gif' border=0><sub>1</sub> 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-<img src='/image/spc_char/beta.gif' border=0><sub>1</sub> stimulates VEGF expression <i style="">in vitro</i> 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-<img src='/image/spc_char/beta.gif' border=0><sub>1</sub> for different time points. Control cells received serum-free culture medium. TGF‑<img src='/image/spc_char/beta.gif' border=0><sub>1, </sub>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-<img src='/image/spc_char/beta.gif' border=0><sub>1</sub> for 4 to 8 h. TGF-<img src='/image/spc_char/beta.gif' border=0><sub>1</sub> 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-<img src='/image/spc_char/beta.gif' border=0><sub>1 </sub>induced VEGF was biologically active. We conclude that TGF-<img src='/image/spc_char/beta.gif' border=0><sub>1 </sub>in addition to an extracellular matrix regulator also could play a key role in bronchial angiogenesis and vascular remodelling via VEGF pathway in asthma. </span>
Description: 262-269
URI: http://hdl.handle.net/123456789/12701
ISSN: 0975-0959 (Online); 0301-1208 (Print)
Appears in Collections:IJBB Vol.48(4) [August 2011]

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