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

doi:10.1186/s12931-017-0711-x

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 journal › Letter (Academic Journal) › peer-review

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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-A_xxxa protein expression was upregulated by hypoxia, mediated through activation of VEGF-A_xxxa 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-A_xxxa isoforms as drivers of fibrogenesis.

Original language	English
Article number	9
Number of pages	5
Journal	Respiratory Research
Volume	19
DOIs	https://doi.org/10.1186/s12931-017-0711-x
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

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

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.",

keywords = "Hypoxia, Idiopathic pulmonary fibrosis, Interstitial lung disease, Vascular endothelial growth factor",

author = "Barratt, {Shaney L.} and Thomas Blythe and Khadija Ourradi and Caroline Jarrett and Welsh, {Gavin I.} and Bates, {David O.} and Millar, {Ann B.}",

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T1 - Effects of hypoxia and hyperoxia on the differential expression of VEGF-A isoforms and receptors in Idiopathic Pulmonary Fibrosis (IPF)

AU - Barratt, Shaney L.

AU - Blythe, Thomas

AU - Ourradi, Khadija

AU - Jarrett, Caroline

AU - Welsh, Gavin I.

AU - Bates, David O.

AU - Millar, Ann B.

PY - 2018/1/15

Y1 - 2018/1/15

N2 - 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.

AB - 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.

KW - Hypoxia

KW - Idiopathic pulmonary fibrosis

KW - Interstitial lung disease

KW - Vascular endothelial growth factor

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U2 - 10.1186/s12931-017-0711-x

DO - 10.1186/s12931-017-0711-x

M3 - Letter (Academic Journal)

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AN - SCOPUS:85040653692

SN - 1465-9921

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JO - Respiratory Research

JF - Respiratory Research

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ER -

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

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