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4 results on '"Caputi, Mario"'

1. Effects of TGF-beta and glucocorticoids on map kinase phosphorylation, IL-6/IL-11 secretion and cell proliferation in primary cultures of human lung fibroblasts.

Author

Pelaia G, Gallelli L, D'Agostino B, Vatrella A, Cuda G, Fratto D, Renda T, Galderisi U, Piegari E, Crimi N, Rossi F, Caputi M, Costanzo FS, Vancheri C, Maselli R, and Marsico SA

Subjects
Cell Proliferation drug effects, Cell Survival drug effects, Cell Survival physiology, Cells, Cultured, Enzyme Activation drug effects, Enzyme Activation physiology, Enzyme Inhibitors pharmacology, Fibroblasts drug effects, Humans, Interleukin-11 metabolism, Interleukin-6 metabolism, Lung drug effects, MAP Kinase Signaling System drug effects, Mitogen-Activated Protein Kinase 1 drug effects, Mitogen-Activated Protein Kinase 1 metabolism, Phosphorylation drug effects, Up-Regulation drug effects, Up-Regulation physiology, Fibroblasts metabolism, Glucocorticoids pharmacology, Interleukins metabolism, Lung metabolism, MAP Kinase Signaling System physiology, Transforming Growth Factor beta1 pharmacology
Abstract

Transforming growth factor-beta1 (TGF-beta1) is crucially involved in the fibrotic events characterizing interstitial lung diseases (ILDs), as well as in the airway remodeling process typical of asthma. Within such a context, the aim of our study was to investigate, in primary cultures of normal and fibrotic human lung fibroblasts (HLFs), the effects of TGF-beta1 on mitogen-activated protein kinase (MAPK) phosphorylation, cell proliferation, and production of interleukins 6 (IL-6) and 11 (IL-11), in the presence or absence of a pretreatment with budesonide (BUD). MAPK phosphorylation was detected by Western blotting, cell viability and proliferation were evaluated using Trypan blue staining and [(3)H]-thymidine incorporation assay, respectively, and the release of IL-6 and IL-11 into cell culture supernatants was assessed by ELISA. TGF-beta1 (10 ng/ml) significantly stimulated MAPK phosphorylation (P < 0.01), and also enhanced cell proliferation as well as the secretion of both IL-6 and IL-11, which reached the highest increases at the 72nd h of cell exposure to this growth factor. All such effects were prevented by BUD (10(-8) M) and, with the exception of IL-6 release, also by a mixture of MAPK inhibitors. Therefore, our findings suggest that the fibrotic action exerted by TGF-beta1 in the lung is mediated at least in part by MAPK activation and by an increased synthesis of the profibrogenic cytokines IL-6 and IL-11; all these effects appear to be prevented by corticosteroids via inhibition of MAPK phosphorylation.

Published
2007
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2. Endothelin-1 induces proliferation of human lung fibroblasts and IL-11 secretion through an ET(A) receptor-dependent activation of MAP kinases.

Author

Gallelli L, Pelaia G, D'Agostino B, Cuda G, Vatrella A, Fratto D, Gioffrè V, Galderisi U, De Nardo M, Mastruzzo C, Salinaro ET, Maniscalco M, Sofia M, Crimi N, Rossi F, Caputi M, Costanzo FS, Maselli R, Marsico SA, and Vancheri C

Subjects
Cell Proliferation drug effects, Cell Survival drug effects, Endothelin A Receptor Antagonists, Endothelin B Receptor Antagonists, Endothelin-1 metabolism, Fibroblasts drug effects, Humans, Interleukin-6 metabolism, Phosphorylation drug effects, RNA, Messenger genetics, RNA, Messenger metabolism, Receptor, Endothelin A genetics, Receptor, Endothelin B genetics, Time Factors, Endothelin-1 pharmacology, Fibroblasts cytology, Fibroblasts metabolism, Interleukin-11 metabolism, Lung cytology, Mitogen-Activated Protein Kinases metabolism, Receptor, Endothelin A metabolism
Abstract

Endothelin-1 (ET-1) is implicated in the fibrotic responses characterizing interstitial lung diseases, as well as in the airway remodeling process occurring in asthma. Within such a context, the aim of our study was to investigate, in primary cultures of normal human lung fibroblasts (NHLFs), the ET-1 receptor subtypes, and the intracellular signal transduction pathways involved in the proliferative effects of this peptide. Therefore, cells were exposed to ET-1 in the presence or absence of an overnight pre-treatment with either ET(A) or ET(B) selective receptor antagonists. After cell lysis, immunoblotting was performed using monoclonal antibodies against the phosphorylated, active forms of mitogen-activated protein kinases (MAPK). ET-1 induced a significant increase in MAPK phosphorylation pattern, and also stimulated fibroblast proliferation and IL-6/IL-11 release into cell culture supernatants. All these effects were inhibited by the selective ET(A) antagonist BQ-123, but not by the specific ET(B) antagonist BQ-788. The stimulatory influence of ET-1 on IL-11, but not on IL-6 secretion, was prevented by MAPK inhibitors. Therefore, such results suggest that in human lung fibroblasts ET-1 exerts a profibrogenic action via an ET(A) receptor-dependent, MAPK-mediated induction of IL-11 release and cell proliferation., (Copyright 2005 Wiley-Liss, Inc.)

Published
2005
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3. Endothelin-1 induces proliferation of human lung fibroblasts and IL-11 secretion through an ET(A) receptor-dependent activation of MAP kinases

Author

Luca Gallelli, Marilisa De Nardo, Carlo Vancheri, Francesco Costanzo, Mario Caputi, Mauro Maniscalco, Giovanni Cuda, Bruno D'Agostino, V. Gioffrè, C. Mastruzzo, Serafino A. Marsico, Matteo Sofia, Francesco Rossi, Girolamo Pelaia, Alessandro Vatrella, Umberto Galderisi, Elisa Trovato Salinaro, Nunzio Crimi, Rosario Maselli, D. Fratto, Gallelli, Luca, Pelaia, Girolamo, D'Agostino, Bruno, Cuda, Giovanni, Vatrella, Alessandro, Fratto, Donatella, Gioffrè, Vincenza, Galderisi, Umberto, De Nardo, Marilisa, Mastruzzo, Claudio, Salinaro, Elisa Trovato, Maniscalco, Mauro, Sofia, Matteo, Crimi, Nunzio, Rossi, Francesco, Caputi, Mario, Costanzo, Francesco S, Maselli, Rosario, Marsico, Serafino A, Vancheri, Carlo, Gallelli, L, Pelaia, G, Cuda, G, Vatrella, A, Fratto, D, Gioffre, V, DE NARDO, M, Mastruzzo, C, Salinaro, Et, Maniscalco, M, Sofia, M, Crimi, N, Rossi, F, Caputi, M, Costanzo, F, Maselli, R, Marsico, Sa, and Vancheri, C.

Subjects
MAPK/ERK pathway, Time Factors, Cell Survival, Endothelin A Receptor Antagonists, Biology, Mitogen-Activated Protein Kinase, Biochemistry, Endothelin B Receptor Antagonist, Humans, Secretion, RNA, Messenger, Phosphorylation, Receptor, Molecular Biology, Lung, Cell Proliferation, IL-6, Endothelin-1, Kinase, Cell growth, Interleukin-6, lung fibroblasts, Cell Biology, ET-1 receptors, Fibroblasts, Interleukin-11, Receptor, Endothelin A, Endothelin 1, MAPK, Receptor, Endothelin B, ET-1, Cell biology, Endothelin B Receptor Antagonists, Intracellular signal transduction, IL-11, Cell culture, Fibroblast, Mitogen-Activated Protein Kinases, Endothelin A Receptor Antagonist, Human
Abstract

Endothelin-1 (ET-1) is implicated in the fibrotic responses characterizing interstitial lung diseases, as well as in the airway remodeling process occurring in asthma. Within such a context, the aim of our study was to investigate, in primary cultures of normal human lung fibroblasts (NHLFs), the ET-1 receptor subtypes, and the intracellular signal transduction pathways involved in the proliferative effects of this peptide. Therefore, cells were exposed to ET-1 in the presence or absence of an overnight pre-treatment with either ETA or ETB selective receptor antagonists. After cell lysis, immunoblotting was performed using monoclonal antibodies against the phosphorylated, active forms of mitogen-activated protein kinases (MAPK). ET-1 induced a significant increase in MAPK phosphorylation pattern, and also stimulated fibroblast proliferation and IL-6/IL-11 release into cell culture supernatants. All these effects were inhibited by the selective ETA antagonist BQ-123, but not by the specific ETB antagonist BQ-788. The stimulatory influence of ET-1 on IL-11, but not on IL-6 secretion, was prevented by MAPK inhibitors. Therefore, such results suggest that in human lung fibroblasts ET-1 exerts a profibrogenic action via an ETA receptor-dependent, MAPK-mediated induction of IL-11 release and cell proliferation. © 2005 Wiley-Liss, Inc.

Published
2005

4. Evidence of angiogenesis in bronchial biopsies of smokers with and without airway obstruction

Author

Carmine Guarino, Carlo Marzo, Vincenzo Bocchino, Alessandro Vatrella, Mario Cazzola, Sergio Mascitti, Pietro Micheli, Mario Caputi, Serafino A. Marsico, Carmelindo M.E. Tranfa, Cecilia Calabrese, Calabrese, C, Bocchino, V, Vatrella, Alessandro, Marzo, C, Guarino, C, Mascitti, S, Tranfa, Cm, Cazzola, M, Micheli, P, Caputi, M, Marsico, Sa, Calabrese, Cecilia, Bocchino, V., Vatrella, A., Marzo, Carlo, Guarino, C., Mascitti, S., Tranfa, Carmelindo Mario Enrico, Cazzola, M., Micheli, P., Caputi, Mario, and Marsico, Serafino Antonio

Subjects
Male, Vascular Endothelial Growth Factor A, Pulmonary and Respiratory Medicine, Pathology, medicine.medical_specialty, Angiogenesis, Biopsy, copd, angiogenesis, VEGF, Integrin αvβ3, smoke, Vital Capacity, Bronchi, Respiratory Mucosa, integrin alpha v beta 3, Neovascularization, chemistry.chemical_compound, Pulmonary Disease, Chronic Obstructive, Forced Expiratory Volume, Smoke, Medicine, Humans, COPD, Bronchus, Lung, Neovascularization, Pathologic, business.industry, Respiratory disease, Smoking, Airway obstruction, Middle Aged, medicine.disease, Integrin alphaVbeta3, respiratory tract diseases, Vascular endothelial growth factor, Angiogenesi, medicine.anatomical_structure, chemistry, Female, medicine.symptom, business
Abstract

The involvement of bronchial vasculature in the airway remodelling occurring in symptomatic smokers with normal lung function and with chronic obstructive pulmonary disease (COPD) has been poorly investigated. An immunohistochemical study was performed on bronchial biopsies taken from 8 non-smokers and 18 smokers divided, according to global health initiative on obstructive lung diseases (GOLD) classification of COPD, into two groups, GOLD 0 and GOLD 2, each of 9 subjects. The number of vessels and the percentage of vascular area in the lamina propria were evaluated by mAb anti-collagen IV. Cellular expression of VEGF and vascular expression of alphavbeta3 integrin were evaluated by the specific monoclonal antibodies. An image processing and analysis system was used to quantify the immunohistochemical data. The number of vessels, the vascular area, the cellular expression of VEGF, the number and percentage of alphavbeta3 positive vessels were significantly higher in GOLD 0 and in GOLD 2 smokers than in non-smokers. The comparison between GOLD 0 and GOLD 2 smokers did show a weak but significantly lower number of vessels in GOLD 2, while the vascular area and the percentage of alphavbeta3 positive vessels did not differ between the two groups. A higher cellular VEGF expression was detected in the GOLD 2 than in the GOLD 0 group. Angiogenesis of bronchial vessels is a component of the airway remodelling occurring in symptomatic smokers with normal lung function and with COPD, it seems independent by the development of airway obstruction and not related to its severity.

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