Effects of hypoxia and hyperoxia on the differential expression of VEGF-A isoforms and receptors in Idiopathic Pulmonary Fibrosis (IPF)

Shaney L. Barratt*, Thomas Blythe, Khadija Ourradi, Caroline Jarrett, Gavin I. Welsh, David O. Bates, Ann B. Millar

*Corresponding author for this work

Research output: Contribution to journalLetter (Academic Journal)

3 Citations (Scopus)
192 Downloads (Pure)

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 languageEnglish
Article number9
Number of pages5
JournalRespiratory Research
Volume19
DOIs
Publication statusPublished - 15 Jan 2018

Keywords

  • Hypoxia
  • Idiopathic pulmonary fibrosis
  • Interstitial lung disease
  • Vascular endothelial growth factor

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