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Vitronectin expression in the airways of subjects with asthma and chronic obstructive pulmonary disease.

Salazar-Peláez LM, Abraham T, Herrera AM, Correa MA, Ortega JE, Paré PD, Seow CY - PLoS ONE (2015)

Bottom Line: The primary cellular source of vitronectin is hepatocytes; it is not known whether resident cells of airways produce vitronectin, even though the glycoprotein has been found in exhaled breath condensate and bronchoalveolar lavage from healthy subjects and patients with interstitial lung disease.Vitronectin was found in the tracheobronchial epithelium from asthmatic, COPD, and control subjects, although its expression was significantly lower in the asthmatic group.The cause for the decreased vitronectin expression in asthma is not clear, however, the reduced concentration of vitronectin in the epithelial/submucosal layer of airways may be linked to airway remodeling.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, Universidad CES, Medellín, Colombia.

ABSTRACT
Vitronectin, a multifunctional glycoprotein, is involved in coagulation, inhibition of the formation of the membrane attack complex (MAC), cell adhesion and migration, wound healing, and tissue remodeling. The primary cellular source of vitronectin is hepatocytes; it is not known whether resident cells of airways produce vitronectin, even though the glycoprotein has been found in exhaled breath condensate and bronchoalveolar lavage from healthy subjects and patients with interstitial lung disease. It is also not known whether vitronectin expression is altered in subjects with asthma and COPD. In this study, bronchial tissue from 7 asthmatic, 10 COPD and 14 control subjects was obtained at autopsy and analyzed by immunohistochemistry to determine the percent area of submucosal glands occupied by vitronectin. In a separate set of experiments, quantitative colocalization analysis was performed on tracheobronchial tissue sections obtained from donor lungs (6 asthmatics, 4 COPD and 7 controls). Vitronectin RNA and protein expressions in bronchial surface epithelium were examined in 12 subjects who undertook diagnostic bronchoscopy. Vitronectin was found in the tracheobronchial epithelium from asthmatic, COPD, and control subjects, although its expression was significantly lower in the asthmatic group. Colocalization analysis of 3D confocal images indicates that vitronectin is expressed in the glandular serous epithelial cells and in respiratory surface epithelial cells other than goblet cells. Expression of the 65-kDa vitronectin isoform was lower in bronchial surface epithelium from the diseased subjects. The cause for the decreased vitronectin expression in asthma is not clear, however, the reduced concentration of vitronectin in the epithelial/submucosal layer of airways may be linked to airway remodeling.

No MeSH data available.


Related in: MedlinePlus

Localization of vitronectin in human bronchial epithelium.Indirect immunoperoxidase staining of paraffin sections from cadaver tissue (healthy control). a) Vitronectin expression in submucosal glands of a mainstem bronchus (arrows), magnification x100. b). Presence of vitronectin in the bronchial surface epithelium (arrows), magnification x100. c-d). Enlarged sections from panels a and b, magnification x400.
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pone.0119717.g002: Localization of vitronectin in human bronchial epithelium.Indirect immunoperoxidase staining of paraffin sections from cadaver tissue (healthy control). a) Vitronectin expression in submucosal glands of a mainstem bronchus (arrows), magnification x100. b). Presence of vitronectin in the bronchial surface epithelium (arrows), magnification x100. c-d). Enlarged sections from panels a and b, magnification x400.

Mentions: The area occupied by vitronectin-positive pixels in the submucosal glands (Fig. 2a and 2c) was confined to serous cells (acini), as demonstrated by superimposition of PAS micrographs on immunohistochemical images (S1 Fig). Vitronectin was present in both HC and diseased subjects. However, the percent area of vitronectin expression was significantly lower in asthma and COPD subjects (p = 0.0010) (Fig. 3) (Table 1). A Dunn´s post test showed there was a difference between HC and COPD subjects (p<0.001). There was no difference in the glandular area or glandular volume fraction (Gvf) in submucosal tissues between the two groups. However, the volume fraction of the vitronectin stained tissue (Vvf) was significantly lower in asthmatic and COPD subjects (p<0.001). The post hoc test showed differences between asthmatic and HC (p = 0.01), as well as between COPD individuals and HC (p<0.001) (Table 1). Besides the submucosal glands, vitronectin expression was also observed in the surface epithelium, especially in the apical zone (Fig. 2b and 2d).


Vitronectin expression in the airways of subjects with asthma and chronic obstructive pulmonary disease.

Salazar-Peláez LM, Abraham T, Herrera AM, Correa MA, Ortega JE, Paré PD, Seow CY - PLoS ONE (2015)

Localization of vitronectin in human bronchial epithelium.Indirect immunoperoxidase staining of paraffin sections from cadaver tissue (healthy control). a) Vitronectin expression in submucosal glands of a mainstem bronchus (arrows), magnification x100. b). Presence of vitronectin in the bronchial surface epithelium (arrows), magnification x100. c-d). Enlarged sections from panels a and b, magnification x400.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4358944&req=5

pone.0119717.g002: Localization of vitronectin in human bronchial epithelium.Indirect immunoperoxidase staining of paraffin sections from cadaver tissue (healthy control). a) Vitronectin expression in submucosal glands of a mainstem bronchus (arrows), magnification x100. b). Presence of vitronectin in the bronchial surface epithelium (arrows), magnification x100. c-d). Enlarged sections from panels a and b, magnification x400.
Mentions: The area occupied by vitronectin-positive pixels in the submucosal glands (Fig. 2a and 2c) was confined to serous cells (acini), as demonstrated by superimposition of PAS micrographs on immunohistochemical images (S1 Fig). Vitronectin was present in both HC and diseased subjects. However, the percent area of vitronectin expression was significantly lower in asthma and COPD subjects (p = 0.0010) (Fig. 3) (Table 1). A Dunn´s post test showed there was a difference between HC and COPD subjects (p<0.001). There was no difference in the glandular area or glandular volume fraction (Gvf) in submucosal tissues between the two groups. However, the volume fraction of the vitronectin stained tissue (Vvf) was significantly lower in asthmatic and COPD subjects (p<0.001). The post hoc test showed differences between asthmatic and HC (p = 0.01), as well as between COPD individuals and HC (p<0.001) (Table 1). Besides the submucosal glands, vitronectin expression was also observed in the surface epithelium, especially in the apical zone (Fig. 2b and 2d).

Bottom Line: The primary cellular source of vitronectin is hepatocytes; it is not known whether resident cells of airways produce vitronectin, even though the glycoprotein has been found in exhaled breath condensate and bronchoalveolar lavage from healthy subjects and patients with interstitial lung disease.Vitronectin was found in the tracheobronchial epithelium from asthmatic, COPD, and control subjects, although its expression was significantly lower in the asthmatic group.The cause for the decreased vitronectin expression in asthma is not clear, however, the reduced concentration of vitronectin in the epithelial/submucosal layer of airways may be linked to airway remodeling.

View Article: PubMed Central - PubMed

Affiliation: School of Medicine, Universidad CES, Medellín, Colombia.

ABSTRACT
Vitronectin, a multifunctional glycoprotein, is involved in coagulation, inhibition of the formation of the membrane attack complex (MAC), cell adhesion and migration, wound healing, and tissue remodeling. The primary cellular source of vitronectin is hepatocytes; it is not known whether resident cells of airways produce vitronectin, even though the glycoprotein has been found in exhaled breath condensate and bronchoalveolar lavage from healthy subjects and patients with interstitial lung disease. It is also not known whether vitronectin expression is altered in subjects with asthma and COPD. In this study, bronchial tissue from 7 asthmatic, 10 COPD and 14 control subjects was obtained at autopsy and analyzed by immunohistochemistry to determine the percent area of submucosal glands occupied by vitronectin. In a separate set of experiments, quantitative colocalization analysis was performed on tracheobronchial tissue sections obtained from donor lungs (6 asthmatics, 4 COPD and 7 controls). Vitronectin RNA and protein expressions in bronchial surface epithelium were examined in 12 subjects who undertook diagnostic bronchoscopy. Vitronectin was found in the tracheobronchial epithelium from asthmatic, COPD, and control subjects, although its expression was significantly lower in the asthmatic group. Colocalization analysis of 3D confocal images indicates that vitronectin is expressed in the glandular serous epithelial cells and in respiratory surface epithelial cells other than goblet cells. Expression of the 65-kDa vitronectin isoform was lower in bronchial surface epithelium from the diseased subjects. The cause for the decreased vitronectin expression in asthma is not clear, however, the reduced concentration of vitronectin in the epithelial/submucosal layer of airways may be linked to airway remodeling.

No MeSH data available.


Related in: MedlinePlus