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Upregulated MicroRNA-185-3p Inhibits the Development of Hyperlipidemia in Rats
1Department of Cardiology, Beijing Chao-yang Hospital, Capital Medical University, Beijing, China.
Introduction:
MicroRNA (miR)-185-3p plays a role in multiple types of cancers, while its underlying function remains obscure in hyperlipidemia. This research was conducted to unravel its function in hyperlipidemia development via modulating mastermind-like 1 (MAML1).
Methods:
The hyperlipidemia rat model was established by feeding with high-fat diet. miR-185-3p and MAML1 levels in hyperlipidemia rats were detected. Adenoviral vectors altering miR-185-3p and MAML1 levels were injected into hyperlipidemia rats to examine the levels of serum lipids, oxidative stress, inflammatory cytokine, lipid accumulation, and cellular morphology in liver tissues of hyperlipidemia rats. The targeting relation between miR-185-3p and MAML1 was manifested.
Results:
miR-185-3p expressed at a low level, while MAML1 expressed at a high level in hyperlipidemia rats. miR-185-3p overexpression or MAML1 silencing reduced levels of serum lipids, mitigated oxidative stress and inflammatory response, and relieved lipid accumulation and pathological morphology in liver tissues in hyperlipidemia rats, while upregulated MAML1 reversed the effects of augmented miR-185-3p in hyperlipidemia rats. Mechanically, miR-185-3p targeted MAML1.
Conclusion:
Upregulated miR-185-3p represses hyperlipidemia development via modulating MAML1 expression. This research provides novel therapeutic candidates for the treatment of hyperlipidemia.
Insights
MicroRNA-185-3p (miR-185-3p) represses hyperlipidemia by downregulating mastermind-like 1 (MAML1). This study reveals miR-185-3p as a potential therapeutic target for hyperlipidemia.
Area of Science:
- Biochemistry
- Molecular Biology
- Genetics
Background:
- MicroRNA (miR)-185-3p is implicated in various cancers.
- Its role in hyperlipidemia pathogenesis is not well understood.
- Mastermind-like 1 (MAML1) is a potential regulator in lipid metabolism.
Purpose of the Study:
- To investigate the function of miR-185-3p in hyperlipidemia.
- To explore the regulatory relationship between miR-185-3p and MAML1 in hyperlipidemia development.
Main Methods:
- A hyperlipidemia rat model was induced using a high-fat diet.
- Levels of miR-185-3p and MAML1 were quantified.
- Adenoviral vectors were used to modulate miR-185-3p and MAML1 expression.
- Serum lipid profiles, oxidative stress markers, inflammatory cytokines, and liver tissue pathology were assessed.
Main Results:
- miR-185-3p expression was decreased, while MAML1 expression was increased in hyperlipidemia rats.
- Overexpression of miR-185-3p or silencing of MAML1 ameliorated hyperlipidemia phenotypes.
- miR-185-3p directly targets MAML1 for regulation.
Conclusions:
- Upregulated miR-185-3p inhibits hyperlipidemia progression by modulating MAML1 expression.
- This study identifies miR-185-3p as a promising therapeutic candidate for hyperlipidemia treatment.
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