التفاصيل البيبلوغرافية
| العنوان: |
Silencing lncRNA NEAT1 reduces nonalcoholic fatty liver fat deposition by regulating the miR-139-5p/c-Jun/SREBP-1c pathway |
| المؤلفون: |
Si-Si Jin, Chun-Jing Lin, Xian-Fan Lin, Ju-Zeng Zheng, Hua-Qin Guan |
| المصدر: |
Annals of Hepatology, Vol 27, Iss 2, Pp 100584- (2022) |
| بيانات النشر: |
Elsevier, 2022. |
| سنة النشر: |
2022 |
| المجموعة: |
LCC:Specialties of internal medicine |
| مصطلحات موضوعية: |
lncRNA NEAT1, miR-139-5p, c-Jun, SREBP1c, Nonalcoholic fatty liver disease, Specialties of internal medicine, RC581-951 |
| الوصف: |
Introduction and Objectives: Nonalcoholic fatty liver disease (NAFLD) starts with the abnormal accumulation of lipids in the liver. Long noncoding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) was reported to modulate hepatic metabolic homeostasis in NAFLD. However, little is known about the molecular mechanisms of NAFLD. Materials and Methods: To establish a NAFLD cellular model, HepG2 cells and LO2 cells were treated with 1 mM free fatty acids (FFAs) for 24 h. NEAT1, miRNA (miR)-139-5p, c-Jun and sterol-regulatory element binding protein-1c (SREBP-1c) were evaluated using qPCR. The protein levels of c-Jun, SREBP1c, acetyl-CoA carboxylase (ACC) and fatty acid synthetase (FAS) were determined using western blotting. Moreover, Oil Red O staining was employed to assess lipid accumulation. In addition, a kit assay was performed to evaluate TG levels. Finally, the interactions among NEAT1, miR-139-5p, c-Jun and SREBP1c were identified by dual luciferase reporter gene assay. Results: NEAT1, c-Jun and SREBP1c expression was markedly elevated, while miR-139-5p expression was reduced in the NAFLD cellular model. NEAT1 knockdown restrained lipid accumulation in the NAFLD cellular model by directly targeting miR-139-5p. Moreover, miR-139-5p overexpression suppressed lipid accumulation by directly suppressing c-Jun expression. In addition, c-Jun silencing suppressed lipid accumulation by directly targeting SREBP1c. Finally, miR-139-5p inhibition mitigated the inhibitory effect of sh-NEAT1 on lipid accumulation. Conclusion: NEAT1 aggravated FFA-induced lipid accumulation in hepatocytes by regulating the c-Jun/SREBP1c axis by sponging miR-139-5p, indicating the potential of NEAT1 as a promising therapeutic target for NAFLD. |
| نوع الوثيقة: |
article |
| وصف الملف: |
electronic resource |
| اللغة: |
English |
| تدمد: |
1665-2681 |
| Relation: |
http://www.sciencedirect.com/science/article/pii/S1665268121002830; https://doaj.org/toc/1665-2681 |
| DOI: |
10.1016/j.aohep.2021.100584 |
| URL الوصول: |
https://doaj.org/article/fb4e84d3a62a4eb88165704458b83c98 |
| رقم الانضمام: |
edsdoj.fb4e84d3a62a4eb88165704458b83c98 |
| قاعدة البيانات: |
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