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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

Vitronectin expression in human bronchial tissues.Expression in submucosal glands (a), and in respiratory surface epithelium (b). The measurements included 7 healthy controls (HC), 6 asthmatic and 4 COPD subjects. For submucosal glands 42 control, 41 asthmatic and 19 COPD acinar structures were evaluated; whereas for respiratory surface epithelium 37 control, 32 asthmatic and 16 COPD tissue structures were assessed. GEA, glandular epithelial area; SEA, surface epithelium area.
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pone.0119717.g007: Vitronectin expression in human bronchial tissues.Expression in submucosal glands (a), and in respiratory surface epithelium (b). The measurements included 7 healthy controls (HC), 6 asthmatic and 4 COPD subjects. For submucosal glands 42 control, 41 asthmatic and 19 COPD acinar structures were evaluated; whereas for respiratory surface epithelium 37 control, 32 asthmatic and 16 COPD tissue structures were assessed. GEA, glandular epithelial area; SEA, surface epithelium area.

Mentions: As mentioned above, stereological analysis of immunohistochemical images from cadaveric tissues showed that vitronectin expression was significantly lower in asthmatic and COPD subjects when compared with the control group. To further quantify the difference we measured pixel intensities of vitronectin per evaluated area of submucosal glands or surface epithelium (with immunofluorescent labeling of vitronectin), on images from 2D optical sections obtained by confocal microscopy of bronchial tissue from lung donors. A total of 109 images were evaluated (average of six per subject). Median values of measurements were obtained for each subject group. Comparisons of results among the three subject groups are shown in Fig. 7. In bronchial submucosal glands, vitronectin expression was lower in asthmatic and COPD individuals when compared with healthy controls. Even though, this difference was only statistically significant for asthmatic individuals versus HC (p<0.0001) (Fig. 7a). The lack of statistical difference between the COPD and control groups could be due to the small sample size of the COPD group (n = 4). There was no difference in the vitronectin expression in the surface epithelium among the groups (Fig. 7b).


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)

Vitronectin expression in human bronchial tissues.Expression in submucosal glands (a), and in respiratory surface epithelium (b). The measurements included 7 healthy controls (HC), 6 asthmatic and 4 COPD subjects. For submucosal glands 42 control, 41 asthmatic and 19 COPD acinar structures were evaluated; whereas for respiratory surface epithelium 37 control, 32 asthmatic and 16 COPD tissue structures were assessed. GEA, glandular epithelial area; SEA, surface epithelium area.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0119717.g007: Vitronectin expression in human bronchial tissues.Expression in submucosal glands (a), and in respiratory surface epithelium (b). The measurements included 7 healthy controls (HC), 6 asthmatic and 4 COPD subjects. For submucosal glands 42 control, 41 asthmatic and 19 COPD acinar structures were evaluated; whereas for respiratory surface epithelium 37 control, 32 asthmatic and 16 COPD tissue structures were assessed. GEA, glandular epithelial area; SEA, surface epithelium area.
Mentions: As mentioned above, stereological analysis of immunohistochemical images from cadaveric tissues showed that vitronectin expression was significantly lower in asthmatic and COPD subjects when compared with the control group. To further quantify the difference we measured pixel intensities of vitronectin per evaluated area of submucosal glands or surface epithelium (with immunofluorescent labeling of vitronectin), on images from 2D optical sections obtained by confocal microscopy of bronchial tissue from lung donors. A total of 109 images were evaluated (average of six per subject). Median values of measurements were obtained for each subject group. Comparisons of results among the three subject groups are shown in Fig. 7. In bronchial submucosal glands, vitronectin expression was lower in asthmatic and COPD individuals when compared with healthy controls. Even though, this difference was only statistically significant for asthmatic individuals versus HC (p<0.0001) (Fig. 7a). The lack of statistical difference between the COPD and control groups could be due to the small sample size of the COPD group (n = 4). There was no difference in the vitronectin expression in the surface epithelium among the groups (Fig. 7b).

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