JAK2/STAT3 Pathway Was Associated with the Protective Effects of IL-22 On Aortic Dissection with Acute Lung Injury

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.

Interleukin-22, a potent target for treatment of non-autoimmune diseases

“…What's more, Wei Ren et al have revealed that the expression of STAT3 in the pulmonary microvascular endothelial cells (PMVECs) after IL-22 interference was obviously increased and the intranuclear accumulation of STAT3 was enhanced, was and these processes were completely inhibited after the interference of AG490, an inhibitor of JAK. 45 Similar results were found in the study by Zhiyong Wu et al The study revealed that IL22 demonstrated protective effects on lung injury through inhibiting AngII-induced PMVECs apoptosis and PMVEC barrier injury by activating the JAK2/ STAT3 signaling pathway.…”

“…The results revealed that IL-22 obviously suppressed the apoptosis of PMVECs mediated by angiotensin II and downregulated the expression and intranuclear transmission of STAT3, and completely inhibited by administration of AG490. 45 Similar to IL-10, recombinant IL-22 treatment inhibited the phenoconversion of alveolar epithelial cells into MFs, thus reducing the number of extracellular matrix producing cells in bleomycin-induced mouse model of lung fibrosis. 47 Administration of anti-IL-22 neutralizing antibody has improved pulmonary inflammation and ECM deposition in the same bleomycininduced model of lung fibrosis.…”

Predictors for the development of preoperative oxygenation impairment in acute aortic dissection in hypertensive patients

“…In ammatory reactions can cause uid to leak across alveolar-capillary barrier because of increased permeability and produce enough alveolar edema to cause the clinical characteristics of refractory hypoxemia [22]. In mice model, IL-22 could signi cantly attenuate the incidence and severity of angiotensin induced acute lung injury [23]. Hence, concerns on anti-in ammatory agents and some protective cytokines will help nd insights on the therapeutic strategy for acute lung injury and OI development in AAD.…”

Corrigendum to “JAK2/STAT3 Pathway Was Associated with the Protective Effects of IL-22 on Aortic Dissection with Acute Lung Injury”

“…The article titled “JAK2/STAT3 Pathway Was Associated with the Protective Effects of IL-22 on Aortic Dissection with Acute Lung Injury” [1] was found to contain material from Wu et al's study [2] and to have missing attributions and errors in citations.…”

“…In addition, there was figure duplication between both articles [1, 2] as follows: The first image in Figure 3(b) in [1] is the same as the second image in Figure 1(c) in [2]The second column in Figure 5 in [1] is the same as the one in Figure 3(b) in [2]…”