Early Activation of Pulmonary TGF-β1/Smad2 Signaling in Mice with Acute Pancreatitis-Associated Acute Lung Injury
Acute lung injury is caused by many factors including acute pancreatitis. There is no specific therapy directed at underlying pathophysiological mechanisms for acute lung injury. Transforming growth factor-β (TGF-β) is involved in the resolution of lung injury in later phases of the disease. Some ev...
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| Format: | Article |
| Language: | English |
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Wiley
2014-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2014/148029 |
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| _version_ | 1832567223373266944 |
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| author | Hamid Akbarshahi Asha Sam Chaolei Chen Ann H. Rosendahl Roland Andersson |
| author_facet | Hamid Akbarshahi Asha Sam Chaolei Chen Ann H. Rosendahl Roland Andersson |
| author_sort | Hamid Akbarshahi |
| collection | DOAJ |
| description | Acute lung injury is caused by many factors including acute pancreatitis. There is no specific therapy directed at underlying pathophysiological mechanisms for acute lung injury. Transforming growth factor-β (TGF-β) is involved in the resolution of lung injury in later phases of the disease. Some evidence exists demonstrating that TGF-β not only is involved in the late stages, but also contributes to lung injury early on in the progress of the disease. Acute pancreatitis was induced using ductal ligation in mice. TGF-β1, 2, and 3, TβRII, ALK-5, Smad2, 3, 4, and 7, and P-Smad2 expression in the lungs were analyzed at 9 and 24 h. We demonstrate that TGF-β1 levels in the lungs of mice with acute pancreatitis increase as early as 9 h after induction. We observed an increased expression of ALK-5 in acute pancreatitis at both 9 and 24 h. Inhibitory Smad7 expression was transiently increased at 9 h in acute pancreatitis, but reduced later at 24 h, with a concomitant increased nuclear translocation of phosphorylated Smad2. Our findings demonstrate activation of TGF-β signaling in the lungs as early as 24 h after acute pancreatitis, suggesting that TGF-β may represent a potential therapeutic candidate in acute pancreatitis-induced acute lung injury. |
| format | Article |
| id | doaj-art-38a599ff3dca411a95c1f5d1bf4ab6eb |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-38a599ff3dca411a95c1f5d1bf4ab6eb2025-02-03T01:02:02ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/148029148029Early Activation of Pulmonary TGF-β1/Smad2 Signaling in Mice with Acute Pancreatitis-Associated Acute Lung InjuryHamid Akbarshahi0Asha Sam1Chaolei Chen2Ann H. Rosendahl3Roland Andersson4Department of Surgery, Clinical Sciences-Lund, Lund University and Skåne University Hospital, 221 85 Lund, SwedenDepartment of Surgery, Clinical Sciences-Lund, Lund University and Skåne University Hospital, 221 85 Lund, SwedenDepartment of Surgery, Clinical Sciences-Lund, Lund University and Skåne University Hospital, 221 85 Lund, SwedenDepartment of Surgery, Clinical Sciences-Lund, Lund University and Skåne University Hospital, 221 85 Lund, SwedenDepartment of Surgery, Clinical Sciences-Lund, Lund University and Skåne University Hospital, 221 85 Lund, SwedenAcute lung injury is caused by many factors including acute pancreatitis. There is no specific therapy directed at underlying pathophysiological mechanisms for acute lung injury. Transforming growth factor-β (TGF-β) is involved in the resolution of lung injury in later phases of the disease. Some evidence exists demonstrating that TGF-β not only is involved in the late stages, but also contributes to lung injury early on in the progress of the disease. Acute pancreatitis was induced using ductal ligation in mice. TGF-β1, 2, and 3, TβRII, ALK-5, Smad2, 3, 4, and 7, and P-Smad2 expression in the lungs were analyzed at 9 and 24 h. We demonstrate that TGF-β1 levels in the lungs of mice with acute pancreatitis increase as early as 9 h after induction. We observed an increased expression of ALK-5 in acute pancreatitis at both 9 and 24 h. Inhibitory Smad7 expression was transiently increased at 9 h in acute pancreatitis, but reduced later at 24 h, with a concomitant increased nuclear translocation of phosphorylated Smad2. Our findings demonstrate activation of TGF-β signaling in the lungs as early as 24 h after acute pancreatitis, suggesting that TGF-β may represent a potential therapeutic candidate in acute pancreatitis-induced acute lung injury.http://dx.doi.org/10.1155/2014/148029 |
| spellingShingle | Hamid Akbarshahi Asha Sam Chaolei Chen Ann H. Rosendahl Roland Andersson Early Activation of Pulmonary TGF-β1/Smad2 Signaling in Mice with Acute Pancreatitis-Associated Acute Lung Injury Mediators of Inflammation |
| title | Early Activation of Pulmonary TGF-β1/Smad2 Signaling in Mice with Acute Pancreatitis-Associated Acute Lung Injury |
| title_full | Early Activation of Pulmonary TGF-β1/Smad2 Signaling in Mice with Acute Pancreatitis-Associated Acute Lung Injury |
| title_fullStr | Early Activation of Pulmonary TGF-β1/Smad2 Signaling in Mice with Acute Pancreatitis-Associated Acute Lung Injury |
| title_full_unstemmed | Early Activation of Pulmonary TGF-β1/Smad2 Signaling in Mice with Acute Pancreatitis-Associated Acute Lung Injury |
| title_short | Early Activation of Pulmonary TGF-β1/Smad2 Signaling in Mice with Acute Pancreatitis-Associated Acute Lung Injury |
| title_sort | early activation of pulmonary tgf β1 smad2 signaling in mice with acute pancreatitis associated acute lung injury |
| url | http://dx.doi.org/10.1155/2014/148029 |
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