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Early Activation of Pulmonary TGF- β 1/Smad2 Signaling in Mice with Acute Pancreatitis-Associated Acute Lung Injury.

Akbarshahi, Hamid LU ; Sam, Asha LU ; Chen, Chaolei LU ; Rosendahl, Ann LU and Andersson, Roland LU (2014) In Mediators of Inflammation 2014(Feb 12).
Abstract
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- β 1, 2, and 3, T β RII, 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- β 1 levels in the lungs of mice with acute pancreatitis increase as early as 9 h... (More)
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- β 1, 2, and 3, T β RII, 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- β 1 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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Mediators of Inflammation
volume
2014
issue
Feb 12
publisher
Hindawi Publishing Corporation
external identifiers
  • pmid:24688224
  • wos:000331766300001
  • scopus:84896383000
ISSN
0962-9351
DOI
10.1155/2014/148029
language
English
LU publication?
yes
id
9430476a-bfc9-4efb-8e3a-4bb9bd07a81e (old id 4431356)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24688224?dopt=Abstract
date added to LUP
2014-05-07 18:42:19
date last changed
2017-08-27 03:00:52
@article{9430476a-bfc9-4efb-8e3a-4bb9bd07a81e,
  abstract     = {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- β 1, 2, and 3, T β RII, 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- β 1 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.},
  articleno    = {148029},
  author       = {Akbarshahi, Hamid and Sam, Asha and Chen, Chaolei and Rosendahl, Ann and Andersson, Roland},
  issn         = {0962-9351},
  language     = {eng},
  number       = {Feb 12},
  publisher    = {Hindawi Publishing Corporation},
  series       = {Mediators of Inflammation},
  title        = {Early Activation of Pulmonary TGF- β 1/Smad2 Signaling in Mice with Acute Pancreatitis-Associated Acute Lung Injury.},
  url          = {http://dx.doi.org/10.1155/2014/148029},
  volume       = {2014},
  year         = {2014},
}