Person: Liao, Mengyang
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Liao
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Mengyang
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Liao, Mengyang
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Publication Allergic lung inflammation promotes atherosclerosis in apolipoprotein E-deficient mice(Elsevier BV, 2016) Liu, Cong-Lin; Wang, Yi; Liao, Mengyang; Santos, Marcela; Fernandes, Cleverson; Sukhova, Galina; Zhang, Jin-Ying; Cheng, Xiang; Yang, Chongzhe; Huang, Xiaozhu; Levy, Bruce; Libby, Peter; Wu, Gongxiong; Shi, Guo-PingInflammation drives asthma and atherosclerosis. Clinical studies suggest that asthmatic patients have a high risk of atherosclerosis. Yet this hypothesis remains uncertain, given that Th2 imbalance causes asthma whereas Th1 immunity promotes atherosclerosis. In this study, chronic allergic lung inflammation (ALI) was induced in mice by ovalbumin sensitization and challenge. Acute ALI was induced in mice by ovalbumin and aluminum sensitization and ovalbumin challenge. Atherosclerosis was produced in apolipoprotein E-deficient (Apoe–/–) mice with a Western diet. When chronic ALI and atherosclerosis were produced simultaneously, ALI increased atherosclerotic lesion size, lesion inflammatory cell content, elastin fragmentation, smooth muscle cell (SMC) loss, lesion cell proliferation, and apoptosis. Production of acute ALI before atherogenesis did not affect lesion size, but increased atherosclerotic lesion CD4+ T cells, lesion SMC loss, angiogenesis, and apoptosis. Production of acute ALI after atherogenesis also did not change atherosclerotic lesion area, but increased lesion elastin fragmentation, cell proliferation, and apoptosis. In mice with chronic ALI and diet-induced atherosclerosis, daily inhalation of a mast cell inhibitor or corticosteroid significantly reduced atherosclerotic lesion T-cell and mast cell contents, SMC loss, angiogenesis, and cell proliferation and apoptosis, although these drugs did not affect lesion area, compared with those that received vehicle treatment. In conclusion, both chronic and acute ALI promote atherogenesis or aortic lesion pathology, regardless whether ALI occurred before, after, or at the same time as atherogenesis. Anti-asthmatic medication can efficiently mitigate atherosclerotic lesion pathology.Publication Interleukin 18 function in atherosclerosis is mediated by the interleukin 18 receptor and the Na-Cl co-transporter(Nature Publishing Group, 2015) Wang, Jing; Sun, Chongxiu; Gerdes, Norbert; Liu, Conglin; Liao, Mengyang; Liu, Jianping; Shi, Michael A; He, Aina; Zhou, Yi; Sukhova, Galina; Chen, Huimei; Cheng, Xiang; Kuzuya, Masafumi; Murohara, Toyoaki; Zhang, Jie; Jiang, Mengmeng; Shull, Gary E; Rogers, Shaunessy; Yang, Chao-Ling; Ke, Q; Jelen, Sabina; Bindels, René; Ellison, David H; Jarolim, Petr; Libby, Peter; Shi, Guo-PingInterleukin-18 (IL18) participates in atherogenesis through several putative mechanisms1, 2. Interruption of IL18 action reduces atherosclerosis in mice3, 4. Here, we show that absence of the IL18 receptor (IL18r) does not affect atherosclerosis in apolipoprotein E–deficient (Apoe−/−) mice, nor does it affect IL18 cell surface binding to or signaling in endothelial cells. As identified initially by co-immunoprecipitation with IL18, we found that IL18 interacts with the Na-Cl co-transporter (NCC; also known as SLC12A3), a 12-transmembrane-domain ion transporter protein preferentially expressed in the kidney5. NCC is expressed in atherosclerotic lesions, where it colocalizes with IL18r. In Apoe−/− mice, combined deficiency of IL18r and NCC, but not single deficiency of either protein, protects mice from atherosclerosis. Peritoneal macrophages from Apoe−/− mice or from Apoe−/− mice lacking IL18r or NCC show IL18 binding and induction of cell signaling and cytokine and chemokine expression, but macrophages from Apoe−/− mice with combined deficiency of IL18r and NCC have a blunted response. An interaction between NCC and IL18r on macrophages was detected by co-immunoprecipitation. IL18 binds to the cell surface of NCC-transfected COS-7 cells, which do not express IL18r, and induces cell signaling and cytokine expression. This study identifies NCC as an IL18-binding protein that collaborates with IL18r in cell signaling, inflammatory molecule expression, and experimental atherogenesis.Publication Allergic Lung Inflammation Aggravates Angiotensin II–Induced Abdominal Aortic Aneurysms in Mice(Ovid Technologies (Wolters Kluwer Health), 2015) Liu, Cong-Lin; Wang, Yi; Liao, Mengyang; Wemmelund, Holger; Ren, Jingyuan; Fernandes, Cleverson; Zhou, Yi; Sukhova, Galina; Lindholt, Jes S.; Johnsen, Søren P.; Zhang, Jin-Ying; Cheng, Xiang; Huang, Xiaozhu; Daugherty, Alan; Levy, Bruce; Libby, Peter; Shi, Guo-PingPublication Deficiency of FcεR1 increases body weight gain but improves glucose tolerance in diet-induced obese mice(Endocrine Society, 2015) Lee, Yun-Jung; Liu, Conglin; Liao, Mengyang; Sukhova, Galina; Shirakawa, Jun; Abdennour, Meriem; Iamarene, Karine; Andre, Sebastien; Inouye, Karen; Clement, Karine; Kulkarni, Rohit; Banks, Alexander; Libby, Peter; Shi, Guo-PingPrior studies demonstrated increased plasma immunoglobulin E (IgE) in diabetic patients, but the direct participation of IgE in diabetes or obesity remains unknown. This study found that plasma IgE levels correlated inversely with body weight, body mass index, and body fat mass among a population of randomly selected obese women. IgE receptor FcεR1-deficient (Fcer1a–/–) mice and diet-induced obesity (DIO) mice demonstrated that FcεR1 deficiency in DIO mice increased food intake, reduced energy expenditure, and increased body weight gain, but improved glucose tolerance and glucose-induced insulin secretion. White adipose tissue (WAT) from Fcer1a–/– mice showed increased expression of phospho-AKT, C/EBPα, PPARγ, Glut4, and Bcl-2, but reduced UCP1 and phospho-JNK expression, tissue macrophage accumulation, and apoptosis, suggesting that IgE reduces adipogenesis and glucose uptake, but induces energy expenditure, adipocyte apoptosis, and WAT inflammation. In 3T3-L1 cells, IgE inhibited the expression of C/EBPα and PPARγ, and preadipocyte adipogenesis, and induced adipocyte apoptosis. IgE reduced 3T3-L1 cell expression of Glut4, phospho-AKT, and glucose uptake, which concurred with improved glucose tolerance in Fcer1a–/– mice. This study established two novel pathways of IgE in reducing body weight gain in DIO mice by suppressing adipogenesis and inducing adipocyte apoptosis, while worsening glucose tolerance by reducing Glut4 expression, glucose uptake, and insulin secretion.Publication Asthma Associates With Human Abdominal Aortic Aneurysm and RuptureSignificance(Ovid Technologies (Wolters Kluwer Health), 2016) Liu, Cong-Lin; Wemmelund, Holger; Wang, Yi; Liao, Mengyang; Lindholt, Jes S.; Johnsen, Søren P.; Vestergaard, Henrik; Fernandes, Cleverson; Sukhova, Galina; Cheng, Xiang; Zhang, Jin-Ying; Yang, Chongzhe; Huang, Xiaozhu; Daugherty, Alan; Levy, Bruce; Libby, Peter; Shi, Guo-PingObjective—Both asthma and abdominal aortic aneurysms (AAA) involve inflammation. It remains unknown whether these diseases interact. Approach and Results—Databases analyzed included Danish National Registry of Patients, a population-based nationwide case–control study included all patients with ruptured AAA and age- and sex-matched AAA controls without rupture in Denmark from 1996 to 2012; Viborg vascular trial, subgroup study of participants from the population-based randomized Viborg vascular screening trial. Patients with asthma were categorized by hospital diagnosis, bronchodilator use, and the recorded use of other anti-asthma prescription medications. Logistic regression models were fitted to determine whether asthma associated with the risk of ruptured AAA in Danish National Registry of Patients and an independent risk of having an AAA at screening in the Viborg vascular trial. From the Danish National Registry of Patients study, asthma diagnosed <1 year or 6 months before the index date increased the risk of AAA rupture before (odds ratio [OR]=1.60–2.12) and after (OR=1.51–2.06) adjusting for AAA comorbidities. Use of bronchodilators elevated the risk of AAA rupture from ever use to within 90 days from the index date, before (OR=1.10–1.37) and after (OR=1.10–1.31) adjustment. Patients prescribed anti-asthma drugs also showed an increased risk of rupture before (OR=1.12–1.79) and after (OR=1.09–1.48) the same adjustment. In Viborg vascular trial, anti-asthmatic medication use associated with increased risk of AAA before (OR=1.45) or after adjustment for smoking (OR=1.45) or other risk factors (OR=1.46). Conclusions—Recent active asthma increased risk of AAA and ruptured AAA. These findings document and furnish novel links between airway disease and AAA, 2 common diseases that share inflammatory aspects.