miR-181d-5p ameliorates hypercholesterolemia by targeting PCSK9.
Yu WangYan-Wen QinXiaoqian GaoHuahui YuZhiyong DuLinyi LiYunhui DuChaowei HuYanwen QinPublished in: The Journal of endocrinology (2024)
Hypercholesterolemia is an independent risk factor for cardiovascular disease and lowering circulating levels of low-density lipoprotein cholesterol (LDL-C) can prevent and reduce cardiovascular events. MicroRNA-181d (miR-181d) can reduce the levels of triglycerides and cholesterol esters in cells. However, it is not known whether miR-181d-5p can lower levels of circulating LDL-C. Here, we generated two animal models of hypercholesterolemia to analyze the potential relationship between miR-181d-5p and LDL-C. In hypercholesterolemia model mice, adeno-associated virus (AAV)-mediated liver-directed overexpression of miR-181d-5p decreased the serum levels of cholesterol and LDL-C and the levels of cholesterol and triglyceride in the liver compared with control mice. Target Scan 8.0 indicated Proprotein convertase subtilisin/kexin type 9 (PCSK9) to be a possible target gene of miR-181d-5p, which was confirmed by in vitro experiments. miR-181d-5p could directly interact with both the PCSK9 3'-UTR and promoter to inhibit PCSK9 translation and transcription. Furthermore, Dil-LDL uptake assays in PCSK9 knockdown Huh7 cells demonstrated that miR-181d-5p promotion of LDL-C absorption was dependent on PCSK9. Collectively, our findings show that miR-181d-5p targets the PCSK9 3'-UTR to inhibit PCSK9 expression and to reduce serum LDL-C. miR-181d-5p is therefore a new therapeutic target for the development of anti-hypercholesterolemia drugs.
Keyphrases
- low density lipoprotein
- cell proliferation
- long non coding rna
- long noncoding rna
- cardiovascular events
- cardiovascular disease
- poor prognosis
- induced apoptosis
- type diabetes
- computed tomography
- magnetic resonance imaging
- skeletal muscle
- metabolic syndrome
- gene expression
- cell death
- dna methylation
- high throughput
- pi k akt
- mouse model
- climate change
- endoplasmic reticulum stress
- signaling pathway
- drug induced