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LncRNA-AK012226 Is Involved in Fat Accumulation in db/db Mice Fatty Liver and Non-alcoholic Fatty Liver Disease Cell Model

Overview of attention for article published in Frontiers in Pharmacology, August 2018
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Title
LncRNA-AK012226 Is Involved in Fat Accumulation in db/db Mice Fatty Liver and Non-alcoholic Fatty Liver Disease Cell Model
Published in
Frontiers in Pharmacology, August 2018
DOI 10.3389/fphar.2018.00888
Pubmed ID
Authors

Xingtian Chen, Yangzhi Xu, Dan Zhao, Ting Chen, Chengxin Gu, Ganxiang Yu, Ken Chen, Yun Zhong, Jie He, Shiming Liu, Yuqiang Nie, Hui Yang

Abstract

Instances of obesity and related metabolic abnormalities are increasing across the world. Non-alcoholic fatty liver disease (NAFLD) is a common disorder in obese people and is becoming the leading cause of hepatocellular carcinoma. Recently, long non-coding RNAs (lncRNAs) have been proven to play remarkable roles in numerous biological processes and human diseases, including NAFLD. However, the function of lncRNA in NAFLD pathogenesis remains largely unknown. The aim of this study was to explore the lncRNA expression profile in NAFLD mice and to identify novel lncRNAs involved in the pathogenesis of NAFLD. We performed microarray analysis to compare the expression profiles of lncRNAs and mRNAs in the liver of diabetic db/db mice with NAFLD and normal mice. A total of 3360 lncRNAs (2048 up-regulated and 1312 down-regulated) and 2685 mRNAs (1195 up-regulated and 1490 down-regulated) were found to be differentially expressed between the NAFLD and control groups. Real-time PCR validation of five differentially expressed lncRNAs in the liver samples was consistent with the microarray results. Besides, the up-regulated lncRNA, AK012226, was also significantly increased in an NCTC1469 NAFLD cellular model. Thus, the up-regulated lncRNA, AK012226, was chosen for subsequent studies. A co-expression network of AK012226-mRNAs was constructed and bioinformatic analysis of these co-expressed mRNAs indicated that they were enriched in the PPAR signaling pathway. Furthermore, Nile red staining and flow cytometry analysis revealed that knockdown of AK012226 by siRNA significantly reduced the lipid accumulation in the NCTC1469 cells treated with free fatty acids. In conclusion, the present study identifies the dysregulated lncRNAs and mRNAs involved in NAFLD, and in particular, a novel lncRNA, AK012226, was identified to be associated with lipid accumulation in NAFLD.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 14 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 14 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 4 29%
Researcher 3 21%
Student > Doctoral Student 1 7%
Student > Master 1 7%
Professor > Associate Professor 1 7%
Other 0 0%
Unknown 4 29%
Readers by discipline Count As %
Medicine and Dentistry 5 36%
Biochemistry, Genetics and Molecular Biology 4 29%
Pharmacology, Toxicology and Pharmaceutical Science 1 7%
Unknown 4 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 26 August 2018.
All research outputs
#20,530,891
of 23,102,082 outputs
Outputs from Frontiers in Pharmacology
#10,331
of 16,458 outputs
Outputs of similar age
#288,975
of 331,157 outputs
Outputs of similar age from Frontiers in Pharmacology
#269
of 383 outputs
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