Skip to content

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

Research output: Contribution to journalLetter

Original languageEnglish
Article number9
Number of pages5
JournalRespiratory Research
Volume19
DOIs
DateAccepted/In press - 26 Dec 2017
DatePublished (current) - 15 Jan 2018

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.

    Research areas

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

Download statistics

No data available

Documents

Documents

  • Full-text PDF (final published version)

    Rights statement: This is the final published version of the article (version of record). It first appeared online via BMC at https://doi.org/10.1186/s12931-017-0711-x . Please refer to any applicable terms of use of the publisher.

    Final published version, 401 KB, PDF document

    Licence: CC BY

DOI

View research connections

Related faculties, schools or groups