TNF-α Regulates Natriuretic Peptides and Aquaporins in Human Bronchial Epithelial Cells BEAS-2B
Postoperative-fluid retention is a severe complication frequently reported in patients undergoing major surgical procedures. The complex network of molecules involved in such a severe surgery-induced condition remains poorly understood. Inflammation has been proposed among the various causes of flui...
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Language: | English |
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Wiley
2013-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2013/159349 |
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author | Letizia Mezzasoma Lucio Cagini Cinzia Antognelli Francesco Puma Eugenio Pacifico Vincenzo Nicola Talesa |
author_facet | Letizia Mezzasoma Lucio Cagini Cinzia Antognelli Francesco Puma Eugenio Pacifico Vincenzo Nicola Talesa |
author_sort | Letizia Mezzasoma |
collection | DOAJ |
description | Postoperative-fluid retention is a severe complication frequently reported in patients undergoing major surgical procedures. The complex network of molecules involved in such a severe surgery-induced condition remains poorly understood. Inflammation has been proposed among the various causes of fluid retention. Since TNF-α is one of the main proinflammatory cytokine initially released after major surgery, it is reasonable to assume its involvement in fluid overload. Here, we showed that TNF-α selectively regulates key molecules involved in fluids balance, such as natriuretic peptides (NPs) and aquaporins, in human bronchial epithelial cells BEAS-2B. In particular, we found that TNF-α induced a decrease of arial natriuretic peptide, natriuretic peptide receptor-1, aquaporin-1 and aquaporin-5 and an increase of brain natriuretic peptide with a different involvement of nuclear factor-κB and mitogen-activated protein kinases signaling pathway activation. Moreover, the observed changes in NPs expression, demonstrate inflammation as an additional cause of brain natriuretic peptide elevation, adding an important piece of information in the novel area of study regarding NPs and inflammation. Finally, we suggest that inflammation is one of the mechanisms of Aquaporin-1 and aquaporin-5 expression regulation. Therefore, in this exploratory study, we speculate that TNF-α might be involved in postoperative-fluid retention related to major surgery. |
format | Article |
id | doaj-art-e2364c6d5f6848be9a248cf15ef56b6f |
institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2013-01-01 |
publisher | Wiley |
record_format | Article |
series | Mediators of Inflammation |
spelling | doaj-art-e2364c6d5f6848be9a248cf15ef56b6f2025-02-03T05:45:15ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/159349159349TNF-α Regulates Natriuretic Peptides and Aquaporins in Human Bronchial Epithelial Cells BEAS-2BLetizia Mezzasoma0Lucio Cagini1Cinzia Antognelli2Francesco Puma3Eugenio Pacifico4Vincenzo Nicola Talesa5Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Polo Unico Sant’Andrea delle Fratte, 06156 Perugia, ItalyThoracic Surgery Unit, Ospedale S. Maria della Misericordia, University of Perugia, S. Andrea delle Fratte, 06156 Perugia, ItalyDepartment of Experimental Medicine and Biochemical Sciences, University of Perugia, Polo Unico Sant’Andrea delle Fratte, 06156 Perugia, ItalyThoracic Surgery Unit, Ospedale S. Maria della Misericordia, University of Perugia, S. Andrea delle Fratte, 06156 Perugia, ItalyClinical Pathology and Hematology Unit, Ospedale S. Maria della Misericordia of Perugia, S. Andrea delle Fratte, 06156 Perugia, ItalyDepartment of Experimental Medicine and Biochemical Sciences, University of Perugia, Polo Unico Sant’Andrea delle Fratte, 06156 Perugia, ItalyPostoperative-fluid retention is a severe complication frequently reported in patients undergoing major surgical procedures. The complex network of molecules involved in such a severe surgery-induced condition remains poorly understood. Inflammation has been proposed among the various causes of fluid retention. Since TNF-α is one of the main proinflammatory cytokine initially released after major surgery, it is reasonable to assume its involvement in fluid overload. Here, we showed that TNF-α selectively regulates key molecules involved in fluids balance, such as natriuretic peptides (NPs) and aquaporins, in human bronchial epithelial cells BEAS-2B. In particular, we found that TNF-α induced a decrease of arial natriuretic peptide, natriuretic peptide receptor-1, aquaporin-1 and aquaporin-5 and an increase of brain natriuretic peptide with a different involvement of nuclear factor-κB and mitogen-activated protein kinases signaling pathway activation. Moreover, the observed changes in NPs expression, demonstrate inflammation as an additional cause of brain natriuretic peptide elevation, adding an important piece of information in the novel area of study regarding NPs and inflammation. Finally, we suggest that inflammation is one of the mechanisms of Aquaporin-1 and aquaporin-5 expression regulation. Therefore, in this exploratory study, we speculate that TNF-α might be involved in postoperative-fluid retention related to major surgery.http://dx.doi.org/10.1155/2013/159349 |
spellingShingle | Letizia Mezzasoma Lucio Cagini Cinzia Antognelli Francesco Puma Eugenio Pacifico Vincenzo Nicola Talesa TNF-α Regulates Natriuretic Peptides and Aquaporins in Human Bronchial Epithelial Cells BEAS-2B Mediators of Inflammation |
title | TNF-α Regulates Natriuretic Peptides and Aquaporins in Human Bronchial Epithelial Cells BEAS-2B |
title_full | TNF-α Regulates Natriuretic Peptides and Aquaporins in Human Bronchial Epithelial Cells BEAS-2B |
title_fullStr | TNF-α Regulates Natriuretic Peptides and Aquaporins in Human Bronchial Epithelial Cells BEAS-2B |
title_full_unstemmed | TNF-α Regulates Natriuretic Peptides and Aquaporins in Human Bronchial Epithelial Cells BEAS-2B |
title_short | TNF-α Regulates Natriuretic Peptides and Aquaporins in Human Bronchial Epithelial Cells BEAS-2B |
title_sort | tnf α regulates natriuretic peptides and aquaporins in human bronchial epithelial cells beas 2b |
url | http://dx.doi.org/10.1155/2013/159349 |
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