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Remodeling of extra-bronchial lung vasculature following allergic airway inflammation.

Rydell-Törmänen, Kristina LU ; Uller, Lena LU and Erjefält, Jonas LU (2008) In Respiratory Research 9(18, FEb 8).
Abstract
BACKGROUND: We previously observed that allergen-exposed mice exhibit remodeling of large bronchial-associated blood vessels. The aim of the study was to examine whether vascular remodeling occurs also in vessels where a spill-over effect of bronchial remodeling molecules is less likely. METHODS: We used an established mouse model of allergic airway inflammation, where an allergic airway inflammation is triggered by inhalations of OVA. Remodeling of bronchial un-associated vessels was determined histologically by staining for alpha-smooth muscle actin, procollagen I, Ki67 and von Willebrand-factor. Myofibroblasts were defined as and visualized by double staining for alpha-smooth muscle actin and procollagen I. For quantification the blood... (More)
BACKGROUND: We previously observed that allergen-exposed mice exhibit remodeling of large bronchial-associated blood vessels. The aim of the study was to examine whether vascular remodeling occurs also in vessels where a spill-over effect of bronchial remodeling molecules is less likely. METHODS: We used an established mouse model of allergic airway inflammation, where an allergic airway inflammation is triggered by inhalations of OVA. Remodeling of bronchial un-associated vessels was determined histologically by staining for alpha-smooth muscle actin, procollagen I, Ki67 and von Willebrand-factor. Myofibroblasts were defined as and visualized by double staining for alpha-smooth muscle actin and procollagen I. For quantification the blood vessels were divided, based on length of basement membrane, into groups; small (</=250 mum) and mid-sized (250-500 mum). RESULTS: We discovered marked remodeling in solitary small and mid-sized blood vessels. Smooth muscle mass increased significantly as did the number of proliferating smooth muscle and endothelial cells. The changes were similar to those previously seen in large bronchial-associated vessels. Additionally, normally poorly muscularized blood vessels changed phenotype to a more muscularized type and the number of myofibroblasts around the small and mid-sized vessels increased following allergen challenge. CONCLUSION: We demonstrate that allergic airway inflammation in mice is accompanied by remodeling of small and mid-sized pulmonary blood vessels some distance away (at least 150 mum) from the allergen-exposed bronchi. The present findings suggest the possibility that allergic airway inflammation may cause such vascular remodeling as previously associated with lung inflammatory conditions involving a risk for development of pulmonary hypertension. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Respiratory Research
volume
9
issue
18, FEb 8
publisher
BioMed Central
external identifiers
  • pmid:18261211
  • wos:000253797000001
  • scopus:41149092973
ISSN
1465-9921
DOI
10.1186/1465-9921-9-18
language
English
LU publication?
yes
id
e85b2b3d-d52c-4ae7-b3c3-e1c8ca8d2e91 (old id 1042119)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18261211?dopt=Abstract
date added to LUP
2008-03-06 16:06:55
date last changed
2017-08-06 04:47:36
@article{e85b2b3d-d52c-4ae7-b3c3-e1c8ca8d2e91,
  abstract     = {BACKGROUND: We previously observed that allergen-exposed mice exhibit remodeling of large bronchial-associated blood vessels. The aim of the study was to examine whether vascular remodeling occurs also in vessels where a spill-over effect of bronchial remodeling molecules is less likely. METHODS: We used an established mouse model of allergic airway inflammation, where an allergic airway inflammation is triggered by inhalations of OVA. Remodeling of bronchial un-associated vessels was determined histologically by staining for alpha-smooth muscle actin, procollagen I, Ki67 and von Willebrand-factor. Myofibroblasts were defined as and visualized by double staining for alpha-smooth muscle actin and procollagen I. For quantification the blood vessels were divided, based on length of basement membrane, into groups; small (&lt;/=250 mum) and mid-sized (250-500 mum). RESULTS: We discovered marked remodeling in solitary small and mid-sized blood vessels. Smooth muscle mass increased significantly as did the number of proliferating smooth muscle and endothelial cells. The changes were similar to those previously seen in large bronchial-associated vessels. Additionally, normally poorly muscularized blood vessels changed phenotype to a more muscularized type and the number of myofibroblasts around the small and mid-sized vessels increased following allergen challenge. CONCLUSION: We demonstrate that allergic airway inflammation in mice is accompanied by remodeling of small and mid-sized pulmonary blood vessels some distance away (at least 150 mum) from the allergen-exposed bronchi. The present findings suggest the possibility that allergic airway inflammation may cause such vascular remodeling as previously associated with lung inflammatory conditions involving a risk for development of pulmonary hypertension.},
  articleno    = {18},
  author       = {Rydell-Törmänen, Kristina and Uller, Lena and Erjefält, Jonas},
  issn         = {1465-9921},
  language     = {eng},
  number       = {18, FEb 8},
  publisher    = {BioMed Central},
  series       = {Respiratory Research},
  title        = {Remodeling of extra-bronchial lung vasculature following allergic airway inflammation.},
  url          = {http://dx.doi.org/10.1186/1465-9921-9-18},
  volume       = {9},
  year         = {2008},
}