Regulation of epithelial cell proliferation by bronchial fibroblasts obtained from mild asthmatic subjects
To cite this article: Semlali A, Jacques E, Rouabhia M, Milot J, Laviolette M, Chakir J. Regulation of epithelial cell proliferation by bronchial fibroblasts obtained from mild asthmatic subjects. Allergy 2010; 65: 1438-1445. Bronchial epithelium is considered a key player in coordinating airway wal...
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| Published in | Allergy (Copenhagen) Vol. 65; no. 11; pp. 1438 - 1445 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Oxford, UK : Blackwell Publishing Ltd
01.11.2010
Blackwell Publishing Ltd Blackwell |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0105-4538 1398-9995 1398-9995 |
| DOI | 10.1111/j.1398-9995.2010.02376.x |
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| Abstract | To cite this article: Semlali A, Jacques E, Rouabhia M, Milot J, Laviolette M, Chakir J. Regulation of epithelial cell proliferation by bronchial fibroblasts obtained from mild asthmatic subjects. Allergy 2010; 65: 1438-1445. Bronchial epithelium is considered a key player in coordinating airway wall remodelling. The function of epithelial cells can be modulated by the underlying fibroblasts through autocrine and paracrine mechanisms. To investigate the effect of phenotypic changes in bronchial fibroblasts from asthmatic subjects on epithelial cell proliferation. Epithelial cells and fibroblasts derived from bronchial biopsies of asthmatic and healthy controls were cultured in an engineered model. Proliferation was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium-bromid (MTT). Epidermal growth factor receptor (EGFR), cyclin-dependent kinase inhibitors p21 and p27 were measured by western blots. Total and active forms of transforming growth factor (TGF)-β₁ were measured using ELISA and bioassay. TGF-β was inhibited using a recombinant TGF-β soluble receptor II protein. Proliferation of epithelial cells from asthmatics (AE) is increased when cells were cultured with fibroblasts from normal controls (NF). Fibroblasts from asthmatics (AF) significantly decreased the proliferation of epithelial cells from healthy subjects (NE). Activation of p21, p27, EGFR and TGF-β₁ reflects the proliferation data by decreasing in AE cultured with NF and increasing in NE cultured with AF. Neutralization of TGF-β increased proliferation of epithelial cells cultured in the asthmatic model. Fibroblasts from asthmatic subjects regulate epithelial cell prolifearation, and TGF-β signalling may represent one of the pathway involved in these interactions. |
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| AbstractList | To cite this article: Semlali A, Jacques E, Rouabhia M, Milot J, Laviolette M, Chakir J. Regulation of epithelial cell proliferation by bronchial fibroblasts obtained from mild asthmatic subjects. Allergy 2010; 65: 1438-1445.AbstractBackground: Bronchial epithelium is considered a key player in coordinating airway wall remodelling. The function of epithelial cells can be modulated by the underlying fibroblasts through autocrine and paracrine mechanisms.Objective: To investigate the effect of phenotypic changes in bronchial fibroblasts from asthmatic subjects on epithelial cell proliferation.Methods: Epithelial cells and fibroblasts derived from bronchial biopsies of asthmatic and healthy controls were cultured in an engineered model. Proliferation was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium-bromid (MTT). Epidermal growth factor receptor (EGFR), cyclin-dependent kinase inhibitors p21 and p27 were measured by western blots. Total and active forms of transforming growth factor (TGF)-b1 were measured using ELISA and bioassay. TGF-b was inhibited using a recombinant TGF-b soluble receptor II protein.Results: Proliferation of epithelial cells from asthmatics (AE) is increased when cells were cultured with fibroblasts from normal controls (NF). Fibroblasts from asthmatics (AF) significantly decreased the proliferation of epithelial cells from healthy subjects (NE). Activation of p21, p27, EGFR and TGF-b1 reflects the proliferation data by decreasing in AE cultured with NF and increasing in NE cultured with AF. Neutralization of TGF-b increased proliferation of epithelial cells cultured in the asthmatic model.Conclusion: Fibroblasts from asthmatic subjects regulate epithelial cell prolifearation, and TGF-b signalling may represent one of the pathway involved in these interactions. To cite this article: Semlali A, Jacques E, Rouabhia M, Milot J, Laviolette M, Chakir J. Regulation of epithelial cell proliferation by bronchial fibroblasts obtained from mild asthmatic subjects. Allergy 2010; 65: 1438-1445. Bronchial epithelium is considered a key player in coordinating airway wall remodelling. The function of epithelial cells can be modulated by the underlying fibroblasts through autocrine and paracrine mechanisms. To investigate the effect of phenotypic changes in bronchial fibroblasts from asthmatic subjects on epithelial cell proliferation. Epithelial cells and fibroblasts derived from bronchial biopsies of asthmatic and healthy controls were cultured in an engineered model. Proliferation was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium-bromid (MTT). Epidermal growth factor receptor (EGFR), cyclin-dependent kinase inhibitors p21 and p27 were measured by western blots. Total and active forms of transforming growth factor (TGF)-β₁ were measured using ELISA and bioassay. TGF-β was inhibited using a recombinant TGF-β soluble receptor II protein. Proliferation of epithelial cells from asthmatics (AE) is increased when cells were cultured with fibroblasts from normal controls (NF). Fibroblasts from asthmatics (AF) significantly decreased the proliferation of epithelial cells from healthy subjects (NE). Activation of p21, p27, EGFR and TGF-β₁ reflects the proliferation data by decreasing in AE cultured with NF and increasing in NE cultured with AF. Neutralization of TGF-β increased proliferation of epithelial cells cultured in the asthmatic model. Fibroblasts from asthmatic subjects regulate epithelial cell prolifearation, and TGF-β signalling may represent one of the pathway involved in these interactions. To cite this article: Semlali A, Jacques E, Rouabhia M, Milot J, Laviolette M, Chakir J. Regulation of epithelial cell proliferation by bronchial fibroblasts obtained from mild asthmatic subjects. Allergy 2010; 65: 1438–1445. Background: Bronchial epithelium is considered a key player in coordinating airway wall remodelling. The function of epithelial cells can be modulated by the underlying fibroblasts through autocrine and paracrine mechanisms. Objective: To investigate the effect of phenotypic changes in bronchial fibroblasts from asthmatic subjects on epithelial cell proliferation. Methods: Epithelial cells and fibroblasts derived from bronchial biopsies of asthmatic and healthy controls were cultured in an engineered model. Proliferation was evaluated by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐tetrazolium‐bromid (MTT). Epidermal growth factor receptor (EGFR), cyclin‐dependent kinase inhibitors p21 and p27 were measured by western blots. Total and active forms of transforming growth factor (TGF)‐β1 were measured using ELISA and bioassay. TGF‐β was inhibited using a recombinant TGF‐β soluble receptor II protein. Results: Proliferation of epithelial cells from asthmatics (AE) is increased when cells were cultured with fibroblasts from normal controls (NF). Fibroblasts from asthmatics (AF) significantly decreased the proliferation of epithelial cells from healthy subjects (NE). Activation of p21, p27, EGFR and TGF‐β1 reflects the proliferation data by decreasing in AE cultured with NF and increasing in NE cultured with AF. Neutralization of TGF‐β increased proliferation of epithelial cells cultured in the asthmatic model. Conclusion: Fibroblasts from asthmatic subjects regulate epithelial cell prolifearation, and TGF‐β signalling may represent one of the pathway involved in these interactions. Background: Bronchial epithelium is considered a key player in coordinating airway wall remodeling. The function of epithelial cells can be modulated by the underlying fibroblasts through autocrine and paracrine mechanisms. Objective: To investigate the effect of phenotypic changes in bronchial fibroblasts from asthmatic subjects on epithelial cell proliferation. Methods: Epithelial cells and fibroblasts derived from bronchial biopsies of asthmatic and healthy controls were cultured in an engineered model. Proliferation was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium-bromid (MTT). Epidermal growth factor receptor (EGFR), cyclin-dependent kinase inhibitors p21 and p27 were measured by western blots. Total and active forms of transforming growth factor (TGF)-β1 were measured using ELISA and bioassay. TGF-β was inhibited using a recombinant TGF-β soluble receptor II protein. Results: Proliferation of epithelial cells from asthmatics (AE) is increased when cells were cultured with fibroblasts from normal controls (NF). Fibroblasts from asthmatics (AF) significantly decreased the proliferation of epithelial cells from healthy subjects (NE). Activation of p21, p27, EGFR and TGF-β1 reflects the proliferation data by decreasing in AE cultured with NF and increasing in NE cultured with AF. Neutralization of TGF-β increased proliferation of epithelial cells cultured in the asthmatic model. Conclusion: Fibroblasts from asthmatic subjects regulate epithelial cell proliferation, and TGF-β signaling may represent one of the pathway involved in these interactions. [PUBLICATION ABSTRACT] Bronchial epithelium is considered a key player in coordinating airway wall remodelling. The function of epithelial cells can be modulated by the underlying fibroblasts through autocrine and paracrine mechanisms. To investigate the effect of phenotypic changes in bronchial fibroblasts from asthmatic subjects on epithelial cell proliferation. Epithelial cells and fibroblasts derived from bronchial biopsies of asthmatic and healthy controls were cultured in an engineered model. Proliferation was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium-bromid (MTT). Epidermal growth factor receptor (EGFR), cyclin-dependent kinase inhibitors p21 and p27 were measured by western blots. Total and active forms of transforming growth factor (TGF)-β₁ were measured using ELISA and bioassay. TGF-β was inhibited using a recombinant TGF-β soluble receptor II protein. Proliferation of epithelial cells from asthmatics (AE) is increased when cells were cultured with fibroblasts from normal controls (NF). Fibroblasts from asthmatics (AF) significantly decreased the proliferation of epithelial cells from healthy subjects (NE). Activation of p21, p27, EGFR and TGF-β₁ reflects the proliferation data by decreasing in AE cultured with NF and increasing in NE cultured with AF. Neutralization of TGF-β increased proliferation of epithelial cells cultured in the asthmatic model. Fibroblasts from asthmatic subjects regulate epithelial cell prolifearation, and TGF-β signalling may represent one of the pathway involved in these interactions. Bronchial epithelium is considered a key player in coordinating airway wall remodelling. The function of epithelial cells can be modulated by the underlying fibroblasts through autocrine and paracrine mechanisms.BACKGROUNDBronchial epithelium is considered a key player in coordinating airway wall remodelling. The function of epithelial cells can be modulated by the underlying fibroblasts through autocrine and paracrine mechanisms.To investigate the effect of phenotypic changes in bronchial fibroblasts from asthmatic subjects on epithelial cell proliferation.OBJECTIVETo investigate the effect of phenotypic changes in bronchial fibroblasts from asthmatic subjects on epithelial cell proliferation.Epithelial cells and fibroblasts derived from bronchial biopsies of asthmatic and healthy controls were cultured in an engineered model. Proliferation was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium-bromid (MTT). Epidermal growth factor receptor (EGFR), cyclin-dependent kinase inhibitors p21 and p27 were measured by western blots. Total and active forms of transforming growth factor (TGF)-β₁ were measured using ELISA and bioassay. TGF-β was inhibited using a recombinant TGF-β soluble receptor II protein.METHODSEpithelial cells and fibroblasts derived from bronchial biopsies of asthmatic and healthy controls were cultured in an engineered model. Proliferation was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium-bromid (MTT). Epidermal growth factor receptor (EGFR), cyclin-dependent kinase inhibitors p21 and p27 were measured by western blots. Total and active forms of transforming growth factor (TGF)-β₁ were measured using ELISA and bioassay. TGF-β was inhibited using a recombinant TGF-β soluble receptor II protein.Proliferation of epithelial cells from asthmatics (AE) is increased when cells were cultured with fibroblasts from normal controls (NF). Fibroblasts from asthmatics (AF) significantly decreased the proliferation of epithelial cells from healthy subjects (NE). Activation of p21, p27, EGFR and TGF-β₁ reflects the proliferation data by decreasing in AE cultured with NF and increasing in NE cultured with AF. Neutralization of TGF-β increased proliferation of epithelial cells cultured in the asthmatic model.RESULTSProliferation of epithelial cells from asthmatics (AE) is increased when cells were cultured with fibroblasts from normal controls (NF). Fibroblasts from asthmatics (AF) significantly decreased the proliferation of epithelial cells from healthy subjects (NE). Activation of p21, p27, EGFR and TGF-β₁ reflects the proliferation data by decreasing in AE cultured with NF and increasing in NE cultured with AF. Neutralization of TGF-β increased proliferation of epithelial cells cultured in the asthmatic model.Fibroblasts from asthmatic subjects regulate epithelial cell prolifearation, and TGF-β signalling may represent one of the pathway involved in these interactions.CONCLUSIONFibroblasts from asthmatic subjects regulate epithelial cell prolifearation, and TGF-β signalling may represent one of the pathway involved in these interactions. |
| Author | Semlali, A Rouabhia, M Jacques, E Milot, J Chakir, J Laviolette, M |
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| Keywords | Human Cell proliferation Lung disease Immunopathology Respiratory disease Dermatology Bronchus epithelial cells Respiratory system Asthma Respiratory tract resident cells Tissue Regulation(control) fibroblasts Immunology engineered bronchial tissue Bronchus disease Epithelial cell Resident (student) Resident Obstructive pulmonary disease Fibroblast |
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| Snippet | To cite this article: Semlali A, Jacques E, Rouabhia M, Milot J, Laviolette M, Chakir J. Regulation of epithelial cell proliferation by bronchial fibroblasts... Bronchial epithelium is considered a key player in coordinating airway wall remodelling. The function of epithelial cells can be modulated by the underlying... Background: Bronchial epithelium is considered a key player in coordinating airway wall remodeling. The function of epithelial cells can be modulated by the... |
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| SubjectTerms | Asthma Asthma - immunology Asthma - metabolism Asthma - pathology Biological and medical sciences biosynthesis Blotting, Western Bronchi Bronchi - immunology Bronchi - metabolism Bronchi - pathology Cell Communication Cell Communication - physiology Cell Proliferation Cells, Cultured Cellular biology Chronic obstructive pulmonary disease, asthma Coculture Techniques Cyclin-Dependent Kinase Inhibitor Proteins Cyclin-Dependent Kinase Inhibitor Proteins - biosynthesis Cyclin-Dependent Kinase Inhibitor Proteins - immunology Dermatology engineered bronchial tissue Enzyme-Linked Immunosorbent Assay epithelial cells Epithelial Cells - immunology Epithelial Cells - metabolism Epithelial Cells - ultrastructure ErbB Receptors fibroblasts Fibroblasts - immunology Fibroblasts - metabolism Fibroblasts - ultrastructure Fundamental and applied biological sciences. Psychology Fundamental immunology Humans immunology Medical sciences metabolism Microscopy, Electron, Scanning pathology physiology Pneumology Receptor, Epidermal Growth Factor - metabolism resident cells Respiratory Mucosa Respiratory Mucosa - immunology Respiratory Mucosa - metabolism Respiratory Mucosa - pathology Reverse Transcriptase Polymerase Chain Reaction Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Signal Transduction Signal Transduction - physiology Tissue Engineering Transforming Growth Factor beta Transforming Growth Factor beta - biosynthesis Transforming Growth Factor beta - immunology ultrastructure |
| Title | Regulation of epithelial cell proliferation by bronchial fibroblasts obtained from mild asthmatic subjects |
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