Abstract
Dysregulation of VEGF-A bioavailability has been implicated in the development of lung injury/fibrosis, exemplified by Idiopathic Pulmonary Fibrosis (IPF). VEGF-A is a target of the hypoxic response via its translational regulation by HIF-1α. The role of hypoxia and hyperoxia in the development and progression of IPF has not been explored. In normal lung (NF) and IPF-derived fibroblasts (FF) VEGF-Axxxa protein expression was upregulated by hypoxia, mediated through activation of VEGF-Axxxa gene transcription. VEGF-A receptors and co-receptors were differentially expressed by hypoxia and hyperoxia. Our data supports a potential role for hypoxia, hyperoxia and VEGF-Axxxa isoforms as drivers of fibrogenesis.
Original language | English |
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Article number | 9 |
Number of pages | 5 |
Journal | Respiratory Research |
Volume | 19 |
DOIs | |
Publication status | Published - 15 Jan 2018 |
Research Groups and Themes
- Academic Respiratory Unit
Keywords
- Hypoxia
- Idiopathic pulmonary fibrosis
- Interstitial lung disease
- Vascular endothelial growth factor