Chemokine localization in bronchial angiogenesis.

Angiogenesis in the lung involves the systemic bronchial vasculature and becomes prominent when chronic inflammation prevails. Mechanisms for neovascularization following pulmonary ischemia include growth factor transit from ischemic parenchyma to upstream bronchial arteries, inflammatory cell migra...

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Main Authors: Maria Grazia Perino, Aigul Moldobaeva, John Jenkins, Elizabeth M Wagner
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2013-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3679055?pdf=render
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author Maria Grazia Perino
Aigul Moldobaeva
John Jenkins
Elizabeth M Wagner
author_facet Maria Grazia Perino
Aigul Moldobaeva
John Jenkins
Elizabeth M Wagner
author_sort Maria Grazia Perino
collection DOAJ
description Angiogenesis in the lung involves the systemic bronchial vasculature and becomes prominent when chronic inflammation prevails. Mechanisms for neovascularization following pulmonary ischemia include growth factor transit from ischemic parenchyma to upstream bronchial arteries, inflammatory cell migration/recruitment through the perfusing artery, and paracrine effects of lung cells within the left bronchus, the niche where arteriogenesis takes place. We analyzed left lung bronchoalveolar lavage (BAL) fluid and left bronchus homogenates after left pulmonary artery ligation (LPAL) in rats, immediately after the onset of ischemia (0 h), 6 h and 24 h later. Additionally, we tested the effectiveness of dexamethasone on decreasing inflammation (0-24 h LPAL) and angiogenesis at early (3 d LPAL; bronchial endothelial proliferation) and late (14 d LPAL; blood flow) stages. After LPAL (6 h), BAL protein, total inflammatory cells, macrophages, and polymorphonuclear cells increased significantly. In parallel, pro-angiogenic CXC chemokines increased in BAL and the left main-stem bronchus (CXCL1) or only within the bronchus (CXCL2). Dexamethasone treatment reduced total BAL protein, inflammatory cells (total and polymorphonuclear cells), and CXCL1 but not CXCL2 in BAL. By contrast, no decrease was seen in either chemokine within the bronchial tissue, in proliferating bronchial endothelial cells, or in systemic perfusion of the left lung. Our results confirm the presence of CXC chemokines within BAL fluid as well as within the left mainstem bronchus. Despite significant reduction in lung injury and inflammation with dexamethasone treatment, chemokine expression within the bronchial tissue as well as angiogenesis were not affected. Our results suggest that early changes within the bronchial niche contribute to subsequent neovascularization during pulmonary ischemia.
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spelling doaj.art-9085afc3909e4fdb85bbe8926a0b0ace2022-12-22T01:29:56ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0186e6643210.1371/journal.pone.0066432Chemokine localization in bronchial angiogenesis.Maria Grazia PerinoAigul MoldobaevaJohn JenkinsElizabeth M WagnerAngiogenesis in the lung involves the systemic bronchial vasculature and becomes prominent when chronic inflammation prevails. Mechanisms for neovascularization following pulmonary ischemia include growth factor transit from ischemic parenchyma to upstream bronchial arteries, inflammatory cell migration/recruitment through the perfusing artery, and paracrine effects of lung cells within the left bronchus, the niche where arteriogenesis takes place. We analyzed left lung bronchoalveolar lavage (BAL) fluid and left bronchus homogenates after left pulmonary artery ligation (LPAL) in rats, immediately after the onset of ischemia (0 h), 6 h and 24 h later. Additionally, we tested the effectiveness of dexamethasone on decreasing inflammation (0-24 h LPAL) and angiogenesis at early (3 d LPAL; bronchial endothelial proliferation) and late (14 d LPAL; blood flow) stages. After LPAL (6 h), BAL protein, total inflammatory cells, macrophages, and polymorphonuclear cells increased significantly. In parallel, pro-angiogenic CXC chemokines increased in BAL and the left main-stem bronchus (CXCL1) or only within the bronchus (CXCL2). Dexamethasone treatment reduced total BAL protein, inflammatory cells (total and polymorphonuclear cells), and CXCL1 but not CXCL2 in BAL. By contrast, no decrease was seen in either chemokine within the bronchial tissue, in proliferating bronchial endothelial cells, or in systemic perfusion of the left lung. Our results confirm the presence of CXC chemokines within BAL fluid as well as within the left mainstem bronchus. Despite significant reduction in lung injury and inflammation with dexamethasone treatment, chemokine expression within the bronchial tissue as well as angiogenesis were not affected. Our results suggest that early changes within the bronchial niche contribute to subsequent neovascularization during pulmonary ischemia.http://europepmc.org/articles/PMC3679055?pdf=render
spellingShingle Maria Grazia Perino
Aigul Moldobaeva
John Jenkins
Elizabeth M Wagner
Chemokine localization in bronchial angiogenesis.
PLoS ONE
title Chemokine localization in bronchial angiogenesis.
title_full Chemokine localization in bronchial angiogenesis.
title_fullStr Chemokine localization in bronchial angiogenesis.
title_full_unstemmed Chemokine localization in bronchial angiogenesis.
title_short Chemokine localization in bronchial angiogenesis.
title_sort chemokine localization in bronchial angiogenesis
url http://europepmc.org/articles/PMC3679055?pdf=render
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AT aigulmoldobaeva chemokinelocalizationinbronchialangiogenesis
AT johnjenkins chemokinelocalizationinbronchialangiogenesis
AT elizabethmwagner chemokinelocalizationinbronchialangiogenesis