Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Mice
Background. Interleukin- (IL-) 22 is considered a proinflammatory cytokine. Recent evidence has demonstrated that it plays a role in cardiovascular diseases. In the recent study, we investigate whether IL-22 is involved in cardiac hypertrophy. Methods. Angiotensin II was used to build hypertrophy mo...
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| Main Authors: | , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2017-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2017/5635929 |
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| author | Jing Ye Ling Liu Qingwei Ji Ying Huang Ying Shi Lei Shi Jianfang Liu Menglong Wang Yao Xu Huimin Jiang Zhen Wang Yingzhong Lin Jun Wan |
| author_facet | Jing Ye Ling Liu Qingwei Ji Ying Huang Ying Shi Lei Shi Jianfang Liu Menglong Wang Yao Xu Huimin Jiang Zhen Wang Yingzhong Lin Jun Wan |
| author_sort | Jing Ye |
| collection | DOAJ |
| description | Background. Interleukin- (IL-) 22 is considered a proinflammatory cytokine. Recent evidence has demonstrated that it plays a role in cardiovascular diseases. In the recent study, we investigate whether IL-22 is involved in cardiac hypertrophy. Methods. Angiotensin II was used to build hypertrophy model and the IL-22 and IL-22 receptor 1 (IL-22R1) levels in heart tissue were measured. In addition, angiotensin II-treated mice received an injection of anti-IL-22-neutralizing antibody (nAb) to investigate the effects of IL-22 nAb on myocardial hypertrophy, cardiac function, and cardiac fibrosis; the activation of the signaling pathway and the prohypertrophic inflammatory cytokine mRNA levels was detected. Furthermore, the effect of IL-22 nAb on angiotensin II-induced hypertrophy in vitro was also determined. Results. IL-22 and IL-22R1 levels were significantly increased after angiotensin II infusion. Anti-IL-22 nAb significantly alleviated the severity of hypertrophy, prevented systolic and diastolic abnormalities, reduced cardiac fibrosis, STAT3 and ERK phosphorylation, and downregulated the mRNA expression of IL-17, IL-6, IL-1β, IFN-γ, and TNF-α. In addition, IL-22 nAb attenuated angiotensin II-induced hypertrophy in H9C2 cells. Conclusion. Our data demonstrated that neutralization of IL-22 alleviated angiotensin II-induced cardiac hypertrophy. The downregulation of IL-22 may be a novel therapeutic strategy to prevent cardiac hypertrophy. |
| format | Article |
| id | doaj-art-325ec05a44a44c119c7f5311cdab891c |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-325ec05a44a44c119c7f5311cdab891c2025-02-03T06:12:44ZengWileyMediators of Inflammation0962-93511466-18612017-01-01201710.1155/2017/56359295635929Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in MiceJing Ye0Ling Liu1Qingwei Ji2Ying Huang3Ying Shi4Lei Shi5Jianfang Liu6Menglong Wang7Yao Xu8Huimin Jiang9Zhen Wang10Yingzhong Lin11Jun Wan12Department of Cardiology, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, ChinaDepartment of Cardiology, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, ChinaDepartment of Cardiology, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, ChinaDepartment of Cardiology, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, ChinaDepartment of Cardiology, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, ChinaDepartment of Cardiology, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, ChinaDepartment of Cardiology, Hubei Key Laboratory of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan University, Wuhan 430060, ChinaDepartment of Cardiology, Hubei Key Laboratory of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan University, Wuhan 430060, ChinaDepartment of Cardiology, Hubei Key Laboratory of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan University, Wuhan 430060, ChinaDepartment of Cardiology, Hubei Key Laboratory of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan University, Wuhan 430060, ChinaDepartment of Cardiology, Hubei Key Laboratory of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan University, Wuhan 430060, ChinaDepartment of Cardiology, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, ChinaDepartment of Cardiology, Hubei Key Laboratory of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan University, Wuhan 430060, ChinaBackground. Interleukin- (IL-) 22 is considered a proinflammatory cytokine. Recent evidence has demonstrated that it plays a role in cardiovascular diseases. In the recent study, we investigate whether IL-22 is involved in cardiac hypertrophy. Methods. Angiotensin II was used to build hypertrophy model and the IL-22 and IL-22 receptor 1 (IL-22R1) levels in heart tissue were measured. In addition, angiotensin II-treated mice received an injection of anti-IL-22-neutralizing antibody (nAb) to investigate the effects of IL-22 nAb on myocardial hypertrophy, cardiac function, and cardiac fibrosis; the activation of the signaling pathway and the prohypertrophic inflammatory cytokine mRNA levels was detected. Furthermore, the effect of IL-22 nAb on angiotensin II-induced hypertrophy in vitro was also determined. Results. IL-22 and IL-22R1 levels were significantly increased after angiotensin II infusion. Anti-IL-22 nAb significantly alleviated the severity of hypertrophy, prevented systolic and diastolic abnormalities, reduced cardiac fibrosis, STAT3 and ERK phosphorylation, and downregulated the mRNA expression of IL-17, IL-6, IL-1β, IFN-γ, and TNF-α. In addition, IL-22 nAb attenuated angiotensin II-induced hypertrophy in H9C2 cells. Conclusion. Our data demonstrated that neutralization of IL-22 alleviated angiotensin II-induced cardiac hypertrophy. The downregulation of IL-22 may be a novel therapeutic strategy to prevent cardiac hypertrophy.http://dx.doi.org/10.1155/2017/5635929 |
| spellingShingle | Jing Ye Ling Liu Qingwei Ji Ying Huang Ying Shi Lei Shi Jianfang Liu Menglong Wang Yao Xu Huimin Jiang Zhen Wang Yingzhong Lin Jun Wan Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Mice Mediators of Inflammation |
| title | Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Mice |
| title_full | Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Mice |
| title_fullStr | Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Mice |
| title_full_unstemmed | Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Mice |
| title_short | Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Mice |
| title_sort | anti interleukin 22 neutralizing antibody attenuates angiotensin ii induced cardiac hypertrophy in mice |
| url | http://dx.doi.org/10.1155/2017/5635929 |
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