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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

(a) Agarose gel electrophoresis of the amplification product for vitronectin cDNA from bronchial brushings.The amplified fragment corresponds to a band size of 151bp. MW, molecular weight marker, Bb, bronchial brushing, and NC, negative control or “non-template control” of qPCR. The number accompanying bronchial brushings corresponds to the number assigned to different patients. (b) Agarose gel electrophoresis of the amplification product for vitronectin cDNA from cultured cells. Molecular weight marker (MW), normal human bronchial epithelial cells (NHBE), cells from adenocarcinoma of epithelial origin (NCL-H23), bronchial brushing (Bb), extraction and retro-transcription control (RT control) or “no reverse-transcriptase control”, and negative control (NC).
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pone.0119717.g008: (a) Agarose gel electrophoresis of the amplification product for vitronectin cDNA from bronchial brushings.The amplified fragment corresponds to a band size of 151bp. MW, molecular weight marker, Bb, bronchial brushing, and NC, negative control or “non-template control” of qPCR. The number accompanying bronchial brushings corresponds to the number assigned to different patients. (b) Agarose gel electrophoresis of the amplification product for vitronectin cDNA from cultured cells. Molecular weight marker (MW), normal human bronchial epithelial cells (NHBE), cells from adenocarcinoma of epithelial origin (NCL-H23), bronchial brushing (Bb), extraction and retro-transcription control (RT control) or “no reverse-transcriptase control”, and negative control (NC).

Mentions: In order to obtain further evidence indicating production of vitronectin by resident cells of the bronchial epithelial layer, vitronectin RNA expression was measured in bronchial brushings, as well as in cell lines of normal human tracheal/bronchial epithelium (primary cells) and lung adenocarcinoma of epithelial origin. A total of 12 bronchial brushings from subjects who underwent diagnostic bronchoscopy were evaluated, with vitronectin coding RNA detected in all of them (Fig. 8a). Vitronectin RNA expression in samples of patients with lung cancer or lung infection was not different compared to the control group (p = 0.281, 95% CI, 0.634–1.159). Transcription of VTN gene was also demonstrated in cultured NHBE and NCL-H23 cells (Fig. 8b). It should be pointed out that the results of our 2-D cell culture may not be the same as those from more physiological 3-D cell cultures.


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)

(a) Agarose gel electrophoresis of the amplification product for vitronectin cDNA from bronchial brushings.The amplified fragment corresponds to a band size of 151bp. MW, molecular weight marker, Bb, bronchial brushing, and NC, negative control or “non-template control” of qPCR. The number accompanying bronchial brushings corresponds to the number assigned to different patients. (b) Agarose gel electrophoresis of the amplification product for vitronectin cDNA from cultured cells. Molecular weight marker (MW), normal human bronchial epithelial cells (NHBE), cells from adenocarcinoma of epithelial origin (NCL-H23), bronchial brushing (Bb), extraction and retro-transcription control (RT control) or “no reverse-transcriptase control”, and negative control (NC).
© Copyright Policy
Related In: Results  -  Collection

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

pone.0119717.g008: (a) Agarose gel electrophoresis of the amplification product for vitronectin cDNA from bronchial brushings.The amplified fragment corresponds to a band size of 151bp. MW, molecular weight marker, Bb, bronchial brushing, and NC, negative control or “non-template control” of qPCR. The number accompanying bronchial brushings corresponds to the number assigned to different patients. (b) Agarose gel electrophoresis of the amplification product for vitronectin cDNA from cultured cells. Molecular weight marker (MW), normal human bronchial epithelial cells (NHBE), cells from adenocarcinoma of epithelial origin (NCL-H23), bronchial brushing (Bb), extraction and retro-transcription control (RT control) or “no reverse-transcriptase control”, and negative control (NC).
Mentions: In order to obtain further evidence indicating production of vitronectin by resident cells of the bronchial epithelial layer, vitronectin RNA expression was measured in bronchial brushings, as well as in cell lines of normal human tracheal/bronchial epithelium (primary cells) and lung adenocarcinoma of epithelial origin. A total of 12 bronchial brushings from subjects who underwent diagnostic bronchoscopy were evaluated, with vitronectin coding RNA detected in all of them (Fig. 8a). Vitronectin RNA expression in samples of patients with lung cancer or lung infection was not different compared to the control group (p = 0.281, 95% CI, 0.634–1.159). Transcription of VTN gene was also demonstrated in cultured NHBE and NCL-H23 cells (Fig. 8b). It should be pointed out that the results of our 2-D cell culture may not be the same as those from more physiological 3-D cell cultures.

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