Design of Specific Peptide Inhibitors for Group I Phospholipase A2:  Structure of a Complex Formed between Phospholipase A2fromNaja naja sagittifera(Group I) and a Designed Peptide Inhibitor Val-Ala-Phe-Arg-Ser (VAFRS) at 1.9 Å Resolution Reveals Unique Features†,‡

Biochemistry ◽  
2003 ◽  
Vol 42 (40) ◽  
pp. 11701-11706 ◽  
Author(s):  
Rajendra Kumar Singh ◽  
P. Vikram ◽  
Jyoti Makker ◽  
Talat Jabeen ◽  
Sujata Sharma ◽  
...  
Pancreas ◽  
1999 ◽  
Vol 18 (1) ◽  
pp. 21-27 ◽  
Author(s):  
E. Kemppainen ◽  
A. Hietaranta ◽  
P. Puolakkainen ◽  
V. Sainio ◽  
J. Halttunen ◽  
...  

Inflammation ◽  
1996 ◽  
Vol 20 (6) ◽  
pp. 599-611 ◽  
Author(s):  
Mats Lindahl ◽  
Christer Tagesson
Keyword(s):  
Group I ◽  

1993 ◽  
Vol 36 (2) ◽  
pp. 96-101 ◽  
Author(s):  
Martti O. Pulkkinen ◽  
Asko I. Kivikoski ◽  
Timo J. Nevalainen

2014 ◽  
Vol 23 (2) ◽  
pp. 140-146 ◽  
Author(s):  
Peng Wang ◽  
Yongtao Li ◽  
Qiuping Shao ◽  
Wenqin Zhou ◽  
Kuifeng Wang

2019 ◽  
Vol 20 (10) ◽  
pp. 2395 ◽  
Author(s):  
Aron B. Fisher ◽  
Chandra Dodia ◽  
Shampa Chatterjee ◽  
Sheldon I. Feinstein

We have previously derived three related peptides, based on a nine-amino acid sequence in human or rat/mouse surfactant protein A, that inhibit the phospholipase A2 activity of peroxiredoxin 6 (Prdx6) and prevent the activation of lung NADPH oxidase (type 2). The present study evaluated the effect of these Prdx6-inhibitory peptides (PIP) in a mouse (C57Bl/6) model of acute lung injury following lipopolysaccharide (LPS) administration. All three peptides (PIP-1, 2 and 3) similarly inhibited the production of reactive O2 species (ROS) in isolated mouse lungs as detected by the oxidation of Amplex red. PIP-2 inhibited both the increased phospholipase A2 activity of Prdx6 and lung reactive oxygen species (ROS) production following treatment of mice with intratracheal LPS (5 µg/g body wt.). Pre-treatment of mice with PIP-2 prevented LPS-mediated lung injury while treatment with PIP-2 at 12 or 16 h after LPS administration led to reversal of lung injury when evaluated 12 or 8 h later, respectively. With a higher dose of LPS (15 µg/g body wt.), mortality was 100% at 48 h in untreated mice but only 28% in mice that were treated at 12–24 h intervals, with PIP-2 beginning at 12 h after LPS administration. Treatment with PIP-2 also markedly decreased mortality after intraperitoneal LPS (15 µg/g body wt.), used as a model of sepsis. This study shows the dramatic effectiveness of a peptide inhibitor of Prdx6 against lung injury and mouse mortality in LPS models. We propose that the PIP nonapeptides may be a useful modality to prevent or to treat human ALI.


2007 ◽  
Vol 50 (24) ◽  
pp. 5938-5950 ◽  
Author(s):  
Maung Maung Thwin ◽  
Seetharama D. Satyanarayanajois ◽  
Latha M. Nagarajarao ◽  
Kazuki Sato ◽  
Pachiappan Arjunan ◽  
...  

2000 ◽  
Vol 17 (7) ◽  
pp. 1010-1021 ◽  
Author(s):  
Kandiah Jeyaseelan ◽  
Arunmozhiarasi Armugam ◽  
Ma Donghui ◽  
Nget-Hong Tan
Keyword(s):  

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