PMID- 31827695 OWN - NLM STAT- MEDLINE DCOM- 20200504 LR - 20200505 IS - 1942-0994 (Electronic) IS - 1942-0900 (Print) IS - 1942-0994 (Linking) VI - 2019 DP - 2019 TI - CD47 Deficiency Attenuates Isoproterenol-Induced Cardiac Remodeling in Mice. PG - 7121763 LID - 10.1155/2019/7121763 [doi] LID - 7121763 AB - In this study, we investigated whether CD47 deficiency attenuates isoproterenol- (ISO-) induced cardiac remodeling in mice. Cardiac remodeling was induced by intraperitoneal (i.p.) injection of ISO (60 mg.kg(-1).d(-1) in 100 mul of sterile normal saline) daily for 14 days and was confirmed by increased levels of lactate dehydrogenase (LDH) and creatine kinase MB (CK-MB), increased heart weight to body weight (HW/BW) ratios, and visible cardiac fibrosis. Apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Levels of malondialdehyde (MDA) and reactive oxygen species (ROS) were found to be significantly higher in the ISO group than in the control group, while superoxide dismutase (SOD) levels were suppressed in the ISO group. However, CD47 knockout significantly limited ISO-induced increases in LDH, CK-MB, and HW/BW ratios, cardiac fibrosis, oxidative stress, and apoptosis in the heart. In addition, CD47 deficiency also increased p-AMPK and LAMP2 expression and decreased HDAC3, cleaved Caspase-3, cleaved Caspase-9, LC3II, and p62 expression in cardiac tissues. In conclusion, CD47 deficiency reduced i.p. ISO-induced cardiac remodeling probably by inhibiting the HDAC3 pathway, improving AMPK signaling and autophagy flux, and rescuing autophagic clearance. CI - Copyright (c) 2019 Zhi Zuo et al. FAU - Zuo, Zhi AU - Zuo Z AUID- ORCID: 0000-0001-8827-3676 AD - Department of Cardiovascular, Zhongda Hospital Affiliated to Southeast University, No. 87 Dingjiaqiao, Nanjing, Jiangsu, China. FAU - Ji, Ming-Yue AU - Ji MY AD - Department of Cardiovascular, Lianshui People's Hospital, No. 6, East Hongri Avenue, Huaian, Jiangsu, China. FAU - Zhao, Kun AU - Zhao K AD - Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, Jiangsu, China. FAU - Su, Zhong-Ping AU - Su ZP AD - Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, Jiangsu, China. FAU - Li, Peng AU - Li P AD - Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, Jiangsu, China. FAU - Hou, Dao-Rong AU - Hou DR AUID- ORCID: 0000-0002-7755-9326 AD - Key Laboratory of Model Animal Research, Animal Core Facility of Nanjing Medical University, Nanjing Medical University, 101 Longmian Avenue, Nanjing, Jiangsu, China. FAU - Li, Yong AU - Li Y AUID- ORCID: 0000-0002-9619-1694 AD - Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, Jiangsu, China. LA - eng PT - Journal Article DEP - 20191119 PL - United States TA - Oxid Med Cell Longev JT - Oxidative medicine and cellular longevity JID - 101479826 RN - 0 (CD47 Antigen) RN - 0 (Cardiotonic Agents) RN - 0 (Cd47 protein, mouse) RN - 0 (Reactive Oxygen Species) RN - L628TT009W (Isoproterenol) SB - IM MH - Animals MH - CD47 Antigen/*physiology MH - Cardiomegaly/chemically induced/pathology/*prevention & control MH - Cardiotonic Agents/*toxicity MH - Isoproterenol/*toxicity MH - Male MH - Mice MH - Mice, Inbred C57BL MH - Mice, Knockout MH - Oxidative Stress/drug effects MH - Reactive Oxygen Species/metabolism MH - Signal Transduction/drug effects MH - Ventricular Remodeling/drug effects/*physiology PMC - PMC6885801 COIS- All authors declare that they have no competing interests. EDAT- 2019/12/13 06:00 MHDA- 2020/05/06 06:00 PMCR- 2019/11/19 CRDT- 2019/12/13 06:00 PHST- 2019/03/17 00:00 [received] PHST- 2019/09/11 00:00 [accepted] PHST- 2019/12/13 06:00 [entrez] PHST- 2019/12/13 06:00 [pubmed] PHST- 2020/05/06 06:00 [medline] PHST- 2019/11/19 00:00 [pmc-release] AID - 10.1155/2019/7121763 [doi] PST - epublish SO - Oxid Med Cell Longev. 2019 Nov 19;2019:7121763. doi: 10.1155/2019/7121763. eCollection 2019.