Limits...
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

Western analysis of vitronectin isoforms expression in bronchial surface epithelium from bronchial brushings.(a) Immunoblots of vitronectin expression in control individuals (number 10, 15 and 17) and diseased subjects (numbers 12, 13, 16, 18, 20, 22, 23, 24 and 25). 65- and 75-kDa vitronectin isoforms are presents in all subjects. β-actin was used as a control for protein loading. (b-c) Quantification by densitometry of 65- and 75-kDa vitronectin isoforms. 65-kDa vitronectin expression was lower in diseased subjects when compared with control individuals (p = 0.0412). The vitronectin/β-actin ratio is represented on the y axes for controls and diseased subjects. Error bars represent the standard error of means.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4358944&req=5

pone.0119717.g009: Western analysis of vitronectin isoforms expression in bronchial surface epithelium from bronchial brushings.(a) Immunoblots of vitronectin expression in control individuals (number 10, 15 and 17) and diseased subjects (numbers 12, 13, 16, 18, 20, 22, 23, 24 and 25). 65- and 75-kDa vitronectin isoforms are presents in all subjects. β-actin was used as a control for protein loading. (b-c) Quantification by densitometry of 65- and 75-kDa vitronectin isoforms. 65-kDa vitronectin expression was lower in diseased subjects when compared with control individuals (p = 0.0412). The vitronectin/β-actin ratio is represented on the y axes for controls and diseased subjects. Error bars represent the standard error of means.

Mentions: To quantitatively evaluate the expression of vitronectin isoforms in bronchial surface epithelial cells, western-blot analysis was carried out in a total of 12 bronchial brushings samples. The vitronectin isoforms were observed in both controls (with normal bronchoscopic, histological and microbiological findings) and diseased subjects (Fig. 9a). Densitometry analysis of vitronectin isoforms on western blots showed that the diseased subjects had decreased expression for the 65-kDa vitronectin isoform when compared with the control group (p = 0.0412) (Fig. 9b). There was no difference in the 75-kDa isoform expression between the two groups (p = 0.1702) (Fig. 9c).


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)

Western analysis of vitronectin isoforms expression in bronchial surface epithelium from bronchial brushings.(a) Immunoblots of vitronectin expression in control individuals (number 10, 15 and 17) and diseased subjects (numbers 12, 13, 16, 18, 20, 22, 23, 24 and 25). 65- and 75-kDa vitronectin isoforms are presents in all subjects. β-actin was used as a control for protein loading. (b-c) Quantification by densitometry of 65- and 75-kDa vitronectin isoforms. 65-kDa vitronectin expression was lower in diseased subjects when compared with control individuals (p = 0.0412). The vitronectin/β-actin ratio is represented on the y axes for controls and diseased subjects. Error bars represent the standard error of means.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0119717.g009: Western analysis of vitronectin isoforms expression in bronchial surface epithelium from bronchial brushings.(a) Immunoblots of vitronectin expression in control individuals (number 10, 15 and 17) and diseased subjects (numbers 12, 13, 16, 18, 20, 22, 23, 24 and 25). 65- and 75-kDa vitronectin isoforms are presents in all subjects. β-actin was used as a control for protein loading. (b-c) Quantification by densitometry of 65- and 75-kDa vitronectin isoforms. 65-kDa vitronectin expression was lower in diseased subjects when compared with control individuals (p = 0.0412). The vitronectin/β-actin ratio is represented on the y axes for controls and diseased subjects. Error bars represent the standard error of means.
Mentions: To quantitatively evaluate the expression of vitronectin isoforms in bronchial surface epithelial cells, western-blot analysis was carried out in a total of 12 bronchial brushings samples. The vitronectin isoforms were observed in both controls (with normal bronchoscopic, histological and microbiological findings) and diseased subjects (Fig. 9a). Densitometry analysis of vitronectin isoforms on western blots showed that the diseased subjects had decreased expression for the 65-kDa vitronectin isoform when compared with the control group (p = 0.0412) (Fig. 9b). There was no difference in the 75-kDa isoform expression between the two groups (p = 0.1702) (Fig. 9c).

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