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

Rydell-Törmänen K, Uller L, Erjefält JS - Respir. Res. (2008)

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Div, Vascular and Airway Research, Dept, Experimental Medical Science, Lund University, Lund, Sweden. Kristina.Rydell-Tormanen@med.lu.se

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 (

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.

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Photomicrographs illustrating vascular remodeling following 7 days of allergen exposure. Vascular remodeling involves smooth muscle (α-smooth muscle actin: red), fibroblasts (procollagen I: brown) and myofibroblasts (here defined as solitary cells co-positive for α-smooth muscle actin and procollagen I: co-positive), in both small solitary (A-B) and mid-sized solitary (C-D) vessels. In comparison with controls (A and C) vessels from OVA exposed animals (B and D) show a significantly increased smooth muscle area as well as increased number of myofibroblasts (arrows) and procollagen I-producing cells. Vascular lumen is indicated by stars. Scale bar represents 50 μm.
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Figure 3: Photomicrographs illustrating vascular remodeling following 7 days of allergen exposure. Vascular remodeling involves smooth muscle (α-smooth muscle actin: red), fibroblasts (procollagen I: brown) and myofibroblasts (here defined as solitary cells co-positive for α-smooth muscle actin and procollagen I: co-positive), in both small solitary (A-B) and mid-sized solitary (C-D) vessels. In comparison with controls (A and C) vessels from OVA exposed animals (B and D) show a significantly increased smooth muscle area as well as increased number of myofibroblasts (arrows) and procollagen I-producing cells. Vascular lumen is indicated by stars. Scale bar represents 50 μm.

Mentions: The perivascular smooth muscle area of mid-sized vessels was significantly increased in animals exposed to allergen (Figures 2 and 3). The increase was at least partially due to hyperplasia, since the number of proliferating smooth muscle cells also increased (1.7 ± 0.6 in controls to 10.8 ± 0.6 cells/mm in allergen exposed animals (p < 0.01)), whereas the number of apoptotic smooth muscle cells did not change (data not shown). Small blood vessels displayed again a similar increase as the mid-sized; the perivascular smooth muscle area increased significantly following allergen exposure (Figures 2 and 3), and thus causing muscularization of partially muscularized blood vessels. The number of proliferating smooth muscle cells was significantly increased in animals exposed to allergen, increasing from 0.1 ± 0.4 cells/mm in controls to 11 ± 0.9 in allergen exposed animals (p < 0.01), the number of apoptotic cells did not change (data not shown).


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

Rydell-Törmänen K, Uller L, Erjefält JS - Respir. Res. (2008)

Photomicrographs illustrating vascular remodeling following 7 days of allergen exposure. Vascular remodeling involves smooth muscle (α-smooth muscle actin: red), fibroblasts (procollagen I: brown) and myofibroblasts (here defined as solitary cells co-positive for α-smooth muscle actin and procollagen I: co-positive), in both small solitary (A-B) and mid-sized solitary (C-D) vessels. In comparison with controls (A and C) vessels from OVA exposed animals (B and D) show a significantly increased smooth muscle area as well as increased number of myofibroblasts (arrows) and procollagen I-producing cells. Vascular lumen is indicated by stars. Scale bar represents 50 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2254605&req=5

Figure 3: Photomicrographs illustrating vascular remodeling following 7 days of allergen exposure. Vascular remodeling involves smooth muscle (α-smooth muscle actin: red), fibroblasts (procollagen I: brown) and myofibroblasts (here defined as solitary cells co-positive for α-smooth muscle actin and procollagen I: co-positive), in both small solitary (A-B) and mid-sized solitary (C-D) vessels. In comparison with controls (A and C) vessels from OVA exposed animals (B and D) show a significantly increased smooth muscle area as well as increased number of myofibroblasts (arrows) and procollagen I-producing cells. Vascular lumen is indicated by stars. Scale bar represents 50 μm.
Mentions: The perivascular smooth muscle area of mid-sized vessels was significantly increased in animals exposed to allergen (Figures 2 and 3). The increase was at least partially due to hyperplasia, since the number of proliferating smooth muscle cells also increased (1.7 ± 0.6 in controls to 10.8 ± 0.6 cells/mm in allergen exposed animals (p < 0.01)), whereas the number of apoptotic smooth muscle cells did not change (data not shown). Small blood vessels displayed again a similar increase as the mid-sized; the perivascular smooth muscle area increased significantly following allergen exposure (Figures 2 and 3), and thus causing muscularization of partially muscularized blood vessels. The number of proliferating smooth muscle cells was significantly increased in animals exposed to allergen, increasing from 0.1 ± 0.4 cells/mm in controls to 11 ± 0.9 in allergen exposed animals (p < 0.01), the number of apoptotic cells did not change (data not shown).

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Div, Vascular and Airway Research, Dept, Experimental Medical Science, Lund University, Lund, Sweden. Kristina.Rydell-Tormanen@med.lu.se

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 (

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.

Show MeSH
Related in: MedlinePlus