当前位置： SCI文献检索 > DIGESTIVE DISEASES AND SCIENCES期刊下所有文献 > CircScd1 Promotes Fatty Liver Disease via the Janus Kinase 2/Signal Transducer and Activator of Transcription 5 Pathway.

CircScd1 Promotes Fatty Liver Disease via the Janus Kinase 2/Signal Transducer and Activator of Transcription 5 Pathway.

Abstract：

BACKGROUND:Nonalcoholic fatty liver disease (NAFLD) is one of the most common liver diseases in affluent countries. Recent studies have reported that circular RNAs (circRNAs) are important regulators of hepatic steatosis. However, the role and mechanism of circRNA in NAFLD are poorly understood. AIMS:This study is to reveal the role and mechanism of circRNA in NAFLD. METHODS:Through NAFLD-related circRNA microarrays, we used real-time quantitative reverse transcription-polymerase chain reaction to screen circScd1 levels in control and test groups of mice fed a high-fat diet. RNA interference and over-expression plasmid vectors were used to manipulate the expression of circScd1, and the biological effects were evaluated by oil red staining, triglyceride detection, and western blot analysis. RESULTS:CircScd1 expression was significantly lower in NAFLD tissues than in control tissues. Moreover, over-expression of circScd1 significantly inhibited the formation of lipid droplets. Western blot analyses showed that the protein levels of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 5 (STAT5) were significantly increased. However, knockdown of circScd1 significantly promoted the degree of hepatocellular lipidosis and reduced the expression levels of JAK2 and STAT5. CONCLUSIONS:Aberrant expression of circScd1 affects the extent of hepatocellular lipidosis in NAFLD and promotes fatty liver disease via the JAK2/STAT5 pathway.

journal_name

Dig Dis Sci

journal_title

Digestive diseases and sciences

authors

Li P,Shan K,Liu Y,Zhang Y,Xu L,Xu L

doi

10.1007/s10620-018-5290-2

subject

Has Abstract

pub_date

2019-01-01 00:00:00

pages

113-122

issue

1

eissn

0163-2116

issn

1573-2568

pii

10.1007/s10620-018-5290-2

journal_volume

64

pub_type

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