Home
|
Inbox
|
Search
|
View Abstract
PP2A Dependent Differential Regulation of MAP Kinase Activation in CSE And LPS Induced Lung Injury
Description
.abstract img { width:300px !important; height:auto; display:block; text-align:center; margin-top:10px } .abstract { overflow-x:scroll } .abstract table { width:100%; display:block; border:hidden; border-collapse: collapse; margin-top:10px } .abstract td, th { border-top: 1px solid #ddd; padding: 4px 8px; } .abstract tbody tr:nth-child(even) td { background-color: #efefef; } .abstract a { overflow-wrap: break-word; word-wrap: break-word; }
A5729 - PP2A Dependent Differential Regulation of MAP Kinase Activation in CSE And LPS Induced Lung Injury
Author Block: R. Wadgaonkar1, A. Majumdar1, A. Bhatt1, A. Dabo2, P. Geraghty3, R. Foronjy1; 1Pulmonary Medicine, Suny Hlth Sci Ctr At Brooklyn, Brooklyn, NY, United States, 2Pulmonary, SUNY Downstate Medical Center, Brooklyn, NY, United States, 3SUNY Downstate, New York, NY, United States.
Introduction: Bacterial endotoxins such as lipopolysaccharides (LPS) and cigarette smoke exacerbates (CSE) acute lung injury by increasing vascular permeability and inflammation. Role of protein phosphatase A (PP2A) has shown to decrease inflammation in chronic lung injury, however the effects of PP2A on acute lung injury from CSE has not been greatly studied. Also the role of PP2A in the regulation of mitogen activated protein kinases (MAPKs) is not clear in cigarette smoke and endotoxin induced lung injury model. Method: Epithelial-A549 cells were stably transfected with control and PP2A siRNA expressing vector. The phosphorylation levels of MAPKs including JNK, ERK, and p38 were compared after LPS and CSE exposure for 30, 60, 120 min. Results: CSE induced ERK activation was enhanced in PP2A negative cells. There was no major difference in LPS induced ERK phosphorylation after inhibition of PP2A. In contrast to that, LPS induced JNK phosphorylation was enhanced after inhibition of PP2A, however CSE induced JNK phosphorylation was not significantly altered after PP2A inhibition. There was significant p38 phosphorylation after 60 min of CSE and LPS treatment but PP2A inhibition did not altered the pattern of p38 phosphorylation. Conclusion: PP2A dependent differential regulation of MAPK activation may have selective role in regulating CSE and LPS induced inflammatory response.
Author Block: R. Wadgaonkar1, A. Majumdar1, A. Bhatt1, A. Dabo2, P. Geraghty3, R. Foronjy1; 1Pulmonary Medicine, Suny Hlth Sci Ctr At Brooklyn, Brooklyn, NY, United States, 2Pulmonary, SUNY Downstate Medical Center, Brooklyn, NY, United States, 3SUNY Downstate, New York, NY, United States.
Introduction: Bacterial endotoxins such as lipopolysaccharides (LPS) and cigarette smoke exacerbates (CSE) acute lung injury by increasing vascular permeability and inflammation. Role of protein phosphatase A (PP2A) has shown to decrease inflammation in chronic lung injury, however the effects of PP2A on acute lung injury from CSE has not been greatly studied. Also the role of PP2A in the regulation of mitogen activated protein kinases (MAPKs) is not clear in cigarette smoke and endotoxin induced lung injury model. Method: Epithelial-A549 cells were stably transfected with control and PP2A siRNA expressing vector. The phosphorylation levels of MAPKs including JNK, ERK, and p38 were compared after LPS and CSE exposure for 30, 60, 120 min. Results: CSE induced ERK activation was enhanced in PP2A negative cells. There was no major difference in LPS induced ERK phosphorylation after inhibition of PP2A. In contrast to that, LPS induced JNK phosphorylation was enhanced after inhibition of PP2A, however CSE induced JNK phosphorylation was not significantly altered after PP2A inhibition. There was significant p38 phosphorylation after 60 min of CSE and LPS treatment but PP2A inhibition did not altered the pattern of p38 phosphorylation. Conclusion: PP2A dependent differential regulation of MAPK activation may have selective role in regulating CSE and LPS induced inflammatory response.
|
Home
|
Inbox
|
Search
|