Mechanism of KLF4 Protection against Acute Liver Injury via Inhibition of Apelin Signaling
Joint Authors
Ji, Weitao
Shi, Hongyun
Shen, Hailin
Kong, Jing
Song, Jiayi
Bian, Hongyan
Lv, Xinrui
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-10, 10 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-10-10
Country of Publication
Egypt
No. of Pages
10
Main Subjects
Abstract EN
Krüppel-like factor 4 (KLF4) is a key transcription factor that regulates genes involved in the proliferation or differentiation in different tissues.
Apelin plays roles in cardiovascular functions, metabolic disease, and homeostatic disorder.
However, the biological function of apelin in liver disease is still ongoing.
In this study, we investigated the mechanism of KLF4-mediated protection against acute liver injury via the inhibition of the apelin signaling pathway.
Mice were intraperitoneally injected with carbon tetrachloride (CCl4; 0.2 mL dissolved in 100 mL olive oil, 10 mL/kg) to establish an acute liver injury model.
A KLF4 expression plasmid was injected through the tail vein 48 h before CCl4 treatment.
In cultured LX-2 cells, pAd-KLF4 or siRNA KLF4 was overexpressed or knockdown, and the mRNA and protein levels of apelin were determined.
The results showed that the apelin serum level in the CCl4-injected group was higher than that of control group, and the expression of apelin in the liver tissues was elevated while KLF4 expression was decreased in the CCl4-injected group compared to the KLF4-plasmid-injected group.
HE staining revealed serious hepatocellular steatosis in the CCl4-injected mice, and KLF4 alleviated this steatosis in the mice injected with KLF4 plasmid.
In vitro experiments showed that tumor necrosis factor-alpha (TNF-α) could downregulate the transcription and translation levels of apelin in LX-2 cells and also upregulate KLF4 mRNA and protein expression.
RT-PCR and Western blotting showed that the overexpression of KLF4 markedly decreased basal apelin expression, but knockdown of KLF4 restored apelin expression in TNF-α-treated LX-2 cells.
These in vivo and in vitro experiments suggest that KLF4 plays a key role in inhibiting hepatocellular steatosis in acute liver injury, and that its mechanism might be the inhibition of the apelin signaling pathway.
American Psychological Association (APA)
Ji, Weitao& Shi, Hongyun& Shen, Hailin& Kong, Jing& Song, Jiayi& Bian, Hongyan…[et al.]. 2019. Mechanism of KLF4 Protection against Acute Liver Injury via Inhibition of Apelin Signaling. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-10.
https://search.emarefa.net/detail/BIM-1204456
Modern Language Association (MLA)
Ji, Weitao…[et al.]. Mechanism of KLF4 Protection against Acute Liver Injury via Inhibition of Apelin Signaling. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-10.
https://search.emarefa.net/detail/BIM-1204456
American Medical Association (AMA)
Ji, Weitao& Shi, Hongyun& Shen, Hailin& Kong, Jing& Song, Jiayi& Bian, Hongyan…[et al.]. Mechanism of KLF4 Protection against Acute Liver Injury via Inhibition of Apelin Signaling. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-10.
https://search.emarefa.net/detail/BIM-1204456
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1204456