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Astrocyte elevated gene‐1 induces autophagy in diabetic cardiomyopathy through upregulation of KLF4
Author(s) -
Zhao Lichun,
Zhang Qianhua,
Liang Jie,
Li Junxiu,
Tan Xiaoming,
Tang g
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28249
Subject(s) - gene knockdown , autophagy , downregulation and upregulation , diabetic cardiomyopathy , neurodegeneration , klf4 , astrocyte , endocrinology , medicine , cardiomyopathy , astrogliosis , biology , cancer research , disease , gene , transcription factor , heart failure , biochemistry , apoptosis , central nervous system , sox2
Background Astrocyte elevated gene‐1 (AEG‐1), also known as metadherin, 3D3, and lysine‐rich carcinoembryonic antigen‐related cell adhesion molecule 1 (CEACAM1) coisolated, has emerged as an important oncogene that is overexpressed in a variety of cancers. Previous studies revealed that AEG‐1 is also involved in multiple physiological and pathological processes, such as development, inflammation, neurodegeneration, migraine, and Huntington's disease. However, the function of AEG‐1 in diabetic cardiomyopathy (DCM) has not been reported yet. Therefore, we conducted this study to characterize the potential role and mechanism of AEG‐1 in DCM rats. Methods DCM was induced by injections of streptozocin (STZ) in Wistar rats. Rats were randomized to be injected with lentivirus carrying AEG‐1 small interfering RNA. Haemodynamic changes of Wistar rats, assessment of cardiac weight index, and the expression of AEG‐1 and KLF4 were detected and compared among these three groups. Results The expressions of AEG‐1 and KLF4 in the STZ group were significantly elevated in cardiac tissues compared with the control group. Knockdown of AEG‐1 significantly increased the values of left ventricular ejection fraction, ±dp/dt max , repressed autophagy, as well as upregulated the expression of KLF4. Conclusions Knockdown of AEG‐1 suppresses autophagy in DCM by downregulating the expression of KLF4. This study provide first‐notion evidence for the potential value of AEG‐1 as a therapeutic target for the treatment of the patients with DCM.