Astrocyte elevated gene-1 induces autophagy in diabetic cardiomyopathy through upregulation of KLF4.


Journal

Journal of cellular biochemistry
ISSN: 1097-4644
Titre abrégé: J Cell Biochem
Pays: United States
ID NLM: 8205768

Informations de publication

Date de publication:
06 2019
Historique:
received: 26 09 2018
accepted: 22 10 2018
pubmed: 7 12 2018
medline: 16 7 2020
entrez: 7 12 2018
Statut: ppublish

Résumé

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. 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. 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 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.

Sections du résumé

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
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.

Identifiants

pubmed: 30520133
doi: 10.1002/jcb.28249
doi:

Substances chimiques

Crisp3 protein, rat 0
Klf4 protein, rat 0
Kruppel-Like Factor 4 0
Kruppel-Like Transcription Factors 0
Membrane Glycoproteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

9709-9715

Informations de copyright

© 2018 Wiley Periodicals, Inc.

Auteurs

Lichun Zhao (L)

Department of Pharmacy, Guangxi University of Chinese Medicine, Nanning, China.

Qianhua Zhang (Q)

Department of Pharmacy, Guangxi University of Chinese Medicine, Nanning, China.

Jie Liang (J)

Department of Pharmacy, Guangxi University of Chinese Medicine, Nanning, China.

Junxiu Li (J)

Department of Pharmacy, Guangxi University of Chinese Medicine, Nanning, China.

Xiaoming Tan (X)

Department of Pharmacy, Guangxi University of Chinese Medicine, Nanning, China.

Nong Tang (N)

Department of Pharmacy, Guangxi University of Chinese Medicine, Nanning, China.

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Classifications MeSH