PRDX2 in Myocyte Hypertrophy and Survival is Mediated by TLR4 in Acute Infarcted Myocardium
Authors: Dandan Li
Yanwen Hang
Peng Zhang
Xian Jin
Qian Su
Wei Hu
Chengjun Chen
Journal: Scientific Reports (2017)
Discipline: Multidisciplinary
Keywords: Peroxiredoxin 2; antioxidant; molecular chaperone; acute myocardial infarction; AMI
Affiliations: Department of Cardiology, Shanghai Minhang Hospital, Fudan University, Shanghai, People's Republic of China., Department of Cardiology, Shanghai Minhang Hospital, Fudan University, Shanghai, People's Republic of China. .

Abstract:  Peroxiredoxin 2 (PRDX2) is an antioxidant and molecular chaperone that can be secreted from tumor cells. But the role of PRDX2 in acute myocardial infarction (AMI) is not clear. In the current study, we demonstrate the role of PRDX2 from clinical trials, H9c2 cells and in a mouse model. ELISA analysis shows that serum concentrations of VEGF and inflammatory factor IL-1Œ≤, TNF-Œ± and IL-6 were increased in AMI patients compared to a control group. The expression of PRDX2 was also upregulated. In vivo experiments show that the expression of PRDX2 inhibits hypoxia-induced oxidative stress injury to H9c2 cells. However, PRDX2 expression promotes TLR4 mediated inflammatory factor expression and VEGF expression under hypoxia conditions. PRDX2 overexpression in H9c2 cells also promotes human endothelial cell migration, vasculogenic mimicry formation and myocardial hypertrophy related protein expression. The overexpression of PRDX2 inhibits ROS level and myocardial injury after AMI but promotes inflammatory responses in vivo. Immunocytochemistry and immunofluorescence analysis show that overexpression of PRDX2 promotes angiogenesis and myocardial hypertrophy. Taken together, our results indicate that PRDX2 plays two roles in acute infarction - the promotion of cell survival and inflammatory myocardial hypertrophy. 

Retracted: No

PubPeer comments:
  Figure 4. PRDX2 overexpression in H9c2 cells promote HUVEC migration, vasculogenic mimicry formation and myocardial hypertrophy related protein expression. H9c2 cells were cultured in serum-free medium and exposed to hypoxic conditions for 6h then in normal conditions for another 24h, then the medium was harvested for transwell and vasculogenic mimicry formation of HUVECs. (A) Migration of HUVECs was assessed using transwell chambers. The invasive capabilities of HUVECs are signifcantly increased with chemotaxis of PRDX2 overexpression in H9c2 cells  I am not convinced that the Hypoxia Control and PRDX2 images really came from different conditions.  Figure 6. The overexpression of PRDX2 promote angiogenesis and myocardial hypertrophy. After 2 weeks of coronary artery ligation, serum from mice was harvested for RT-PCR analysis and myocardial tissue were harvested 4 weeks after artery ligation for immunohistochemical analysis. (A) Effects of PRDX2 on cell surface area of cardiomyocytes. It is unlikely that the tissue samples for AB WT and AB PRDX2 in fact came from different mice.  , 
 #1 Thank you for your attention to our research. We are very grateful for the problems you found. We have carefully studied and reviewed our previous pictures and found that the pictures and annotations were carelessly misplaced. Now we have made the amendment. Please review it. Thank you again for all the trouble you ve taken. , 
 #1 Thank you for your attention to our research. We are very grateful for the problems you found. We have carefully studied and reviewed our previous pictures and found that the pictures and annotations were carelessly misplaced. Now we have made the amendment. Please review it. Thank you again for all the trouble you ve taken. figure 4 . , 
 #1 Thank you for your attention to our research. We are very grateful for the problems you found. We have carefully studied and reviewed our previous pictures and found that the pictures and annotations were carelessly misplaced. Now we have made the amendment. Please review it. Thank you again for all the trouble you ve taken. Figure 6 , 
 Excellent! Thank you for taking the trouble to make the correction. ,