JAK2/STAT3 Pathway Was Associated with the Protective Effects of IL-22 On Aortic Dissection with Acute Lung Injury
Authors: Bowen Li
Jinxing Chang
Feifeng Dai
Zhiyong Wu
Wei Ren
Yongle Ruan
Zhiwei Wang
Zhipeng Hu
Huagang Liu
Journal: Disease markers (2017)
Discipline: CLINICAL MEDICINE
Keywords: aortic dissection; acute lung injury; IL-22; pathogenesis; ALI
Affiliations: Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China., Hubei Key Laboratory of Cardiology, Wuhan 430060, China.

Abstract:  Patients with aortic dissection (AD) may present acute lung injury (ALI) that may affect the prognosis. In this study, we aim to investigate the roles and mechanism of IL-22 in the pathogenesis of AD complicated with ALI. Six hundred and twenty-one AD patients were included, and the incidence of ALI and pulmonary CT findings were analyzed. Mouse ALI model was established through AngII, and then IL-22 injection and AG490 were given. The pathological changes, infiltration of inflammatory cells, and expression of STAT3 were determined. For the in vitro experiment, cultivated pulmonary microvascular endothelial cells (PMVECs) were treated by angiotensin II (AngII), followed by treating with IL-22 and/or AG490. The expression and migration of STAT3 was determined. Flow cytometry was carried out to evaluate the apoptosis. IL-22 contributed to the expression of STAT3 in lung tissues and attenuation of ALI. IL-22 obviously inhibited the apoptosis of PMVECs mediated by AngII and downregulated the expression and intranuclear transmission of STAT3. Such phenomenon was completely inhibited upon administration of AG490, an inhibitor of JAK2. Our data showed IL-22 contributed to the inhibition of PMVEC apoptosis mediated by AngII through activating the JAK2/STAT3 signaling pathway, which may attenuate the ALI induced by AngII. 

Retracted: No

PubPeer comments:
 Could the author explain why the MW of beta actin shown in this figure is 36 kDa instead than the canonical 42 kDa? Also, the MW of PCNA is reported to be 42 kDa instead than 36 kDa. While the two MW could have been reversed by error, the two proteins, unexpectely, migrate accordingly to the their non-canonical molecular weight (see figure).  , 
 The molecular weight of beta actin is 42 KDa not 36. Please amend the figures in this manuscript.  , 
 Molecular weights of beta-actin and PCNA are reversed. However, the proteins seem to have migrated in the correct manner (i.e.beta actin in the up and PCNA in the bottom).  , 
 Similar error in beta-actin m.w. Also these images are likely coming from different sources. Could the authors provide the uncropped scans for these blots?.  , 
 Duplicated beta actins in Figure 6 and 7. Squares of same color identify similar beta actins. The large squares highlight discrepancy of run patterns of beta actins and AKT and pAKT, suggesting that AKT and beta actins are from different sources. Additionally, arrows denote a likely vertical splicing that needs to be checked. Could the authors provide the uncropepd images used to prepare these panels?  , 
 Duplicatede beta actin in Figure 2C and Figure 4. The beta actin in Figure 4 is the upper part of Figure 2C. This exclude that AKT was stripped and reprobed for beta actin as the Figure 4 seem to suggest.  , 
 Figure 4 and Figure 7B, same AKT but experimental settings are different.  , 
 The image below has been rotated by 1u00b0  , 
 Images were reused in two publications by some of the same authors in 2003 and 2007.    ,