单位：[1]Emergency & Critical Care Center, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China首都医科大学附属安贞医院[2]Beijing Institute of Heart, Lung, and Blood Vessel Diseases, Beijing, China首都医科大学附属安贞医院[3]Department of Cardiology, China-Japan Friendship Hospital, Beijing, China
Cardiac rupture is a fatal complication of acute myocardial infarction (MI), associated with increased inflammation and damaged extracellular matrix. C57BL/6 J wild type (WT) and Pde5a knockout (Pde5a(-/-)) mice were selected to establish MI model. The rupture rate of Pde5a(-/-) mice was significantly reduced (P < 0.01) within 7 days post MI. The cardiac function of Pde5a(-/-) mice was better than WT mice both at day 3 and 7 post MI. Immunohistochemical staining and flow cytometry showed neutrophils and macrophages were decreased in Pde5a(-/-) mouse hearts. Inflammatory factors expression such as IL-1 beta, IL-6, IL-8, Mcp-1, TNF-alpha significantly decreased in Pde5a(-/-) mice post MI. Moreover, western blot showed the inhibition of inflammatory response was accompanied by down-regulation of intercellular adhesion molecule-1(ICAM-1) and vascular cell adhesion molecule-1(VCAM-1) in Pde5a(-/-) mice. Knockout of Pde5a reduced inflammatory cells infiltration by down-regulating the expression of ICAM-1 and VCAM-1, and prevented early cardiac rupture after MI. All authors declare that they have no conflicts of interest. This article does not contain any studies with human participants performed by any of the authors. All applicable international, national, and institutional guidelines for the care and use of animals were followed.
基金：
National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81970292, 81600213, 81670222, 81700262]; Beijing Natural Science FoundationBeijing Natural Science Foundation [7191002]; Beijing Hospitals Authority Youth Program [QML20190603]; Capital's Funds for Health Improvement and Research [2018-1-2061]; CS Optimizing Antithrombotic Research Fund [BJUHFCSOARF201901-08]; Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support [ZYLX201710]; Beijing Municipal Administration of Hospitals' Ascent Plan [DFL20180601]
语种：
外文
被引次数：
WOS：
PubmedID：
中科院(CAS)分区：
出版当年[2020]版：
大类|3 区医学
小类|3 区心脏和心血管系统4 区医学：研究与实验
最新[2025]版：
大类|4 区医学
小类|4 区心脏和心血管系统4 区医学：研究与实验
JCR分区：
出版当年[2019]版：
Q2MEDICINE, RESEARCH & EXPERIMENTALQ2CARDIAC & CARDIOVASCULAR SYSTEMS
最新[2023]版：
Q2CARDIAC & CARDIOVASCULAR SYSTEMSQ3MEDICINE, RESEARCH & EXPERIMENTAL
第一作者单位：[1]Emergency & Critical Care Center, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China[2]Beijing Institute of Heart, Lung, and Blood Vessel Diseases, Beijing, China
通讯作者：
通讯机构：[1]Emergency & Critical Care Center, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China[2]Beijing Institute of Heart, Lung, and Blood Vessel Diseases, Beijing, China
推荐引用方式(GB/T 7714)：
Siyi Li,Youcai Ma,Yan Yan,et al.Phosphodiesterase-5a Knock-out Suppresses Inflammation by Down-Regulating Adhesion Molecules in Cardiac Rupture Following Myocardial Infarction[J].JOURNAL of CARDIOVASCULAR TRANSLATIONAL RESEARCH.2021,14(5):816-823.doi:10.1007/s12265-021-10102-2.
APA：
Siyi Li,Youcai Ma,Yan Yan,Mengwen Yan,Xiao Wang...&Shaoping Nie.(2021).Phosphodiesterase-5a Knock-out Suppresses Inflammation by Down-Regulating Adhesion Molecules in Cardiac Rupture Following Myocardial Infarction.JOURNAL of CARDIOVASCULAR TRANSLATIONAL RESEARCH,14,(5)
MLA：
Siyi Li,et al."Phosphodiesterase-5a Knock-out Suppresses Inflammation by Down-Regulating Adhesion Molecules in Cardiac Rupture Following Myocardial Infarction".JOURNAL of CARDIOVASCULAR TRANSLATIONAL RESEARCH 14..5(2021):816-823
