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Updated: May 10, 2026
07:36
Angiogenesis in the Ischemic Rat Lung
Published on: February 8, 2013
Chemokine localization in bronchial angiogenesis.
Maria Grazia Perino1, Aigul Moldobaeva, John Jenkins
1Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, United States of America.
Plos One
|June 19, 2013
Summary
Pulmonary ischemia triggers lung inflammation and angiogenesis. Early bronchial niche changes, not systemic inflammation, drive neovascularization, even after dexamethasone treatment reduces lung injury.
Area of Science:
- Pulmonary vascular remodeling
- Inflammatory signaling in the lung
- Tissue neovascularization mechanisms
Background:
- Angiogenesis in the lung is linked to chronic inflammation and involves the bronchial vasculature.
- Pulmonary ischemia can induce neovascularization through complex mechanisms involving growth factors and inflammatory cells.
- The left bronchus serves as a niche for arteriogenesis, the process of new artery formation.
Purpose of the Study:
- To investigate the mechanisms of neovascularization following pulmonary ischemia.
- To analyze the role of the bronchial niche and inflammatory mediators in angiogenesis after left pulmonary artery ligation (LPAL).
- To evaluate the efficacy of dexamethasone in modulating inflammation and angiogenesis.
Main Methods:
- Rats underwent left pulmonary artery ligation (LPAL) to induce pulmonary ischemia.
- Bronchoalveolar lavage (BAL) fluid and left bronchus homogenates were collected at 0, 6, and 24 hours post-LPAL.
- Dexamethasone treatment was assessed for its effects on inflammation and angiogenesis at early (3 days) and late (14 days) stages post-LPAL.
Main Results:
- LPAL led to increased BAL protein, inflammatory cells (macrophages, polymorphonuclear cells), and pro-angiogenic CXC chemokines (CXCL1, CXCL2) in BAL and bronchial tissue.
- Dexamethasone reduced BAL protein and inflammatory cells, and CXCL1 in BAL, but did not affect CXCL2 in BAL or bronchial tissue.
- Neither chemokine levels in bronchial tissue nor bronchial endothelial proliferation or lung perfusion were reduced by dexamethasone.
Conclusions:
- Early changes within the bronchial niche, including chemokine expression, contribute to neovascularization during pulmonary ischemia.
- Dexamethasone effectively reduces lung injury and inflammation but does not inhibit angiogenesis or bronchial chemokine expression in this model.
- These findings highlight the localized nature of early angiogenic responses within the bronchial niche following pulmonary ischemia.
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