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Updated: Dec 10, 2025

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
Hsa_circ_0000345 regulates the cellular development of ASMCs in response to oxygenized low-density lipoprotein
Huifang Liu1, Xiaowen Ma1, Xin Wang1
1Department of Endocrinology and Metabolism, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Insights
This study reveals that hsa_circ_0000345 protects aortic smooth muscle cells from damage caused by oxidized low-density lipoprotein (ox-LDL), a key factor in atherosclerosis. Upregulating this circRNA enhances cell viability and inhibits apoptosis in atherosclerosis models.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Epigenetics
Background:
- Atherosclerosis involves complex cellular and molecular interactions.
- Circular RNAs (circRNAs) are increasingly recognized for their roles in disease regulation.
- Novel circRNAs require investigation to fully understand atherosclerosis pathogenesis.
Purpose of the Study:
- To investigate the role of hsa_circ_0000345 in the cellular development of atherosclerosis.
- To determine the regulatory effect of hsa_circ_0000345 on oxygenized low-density lipoprotein (ox-LDL)-treated aortic smooth muscle cells (ASMCs).
Main Methods:
- ASMCs were treated with ox-LDL to induce an atherosclerosis model.
- hsa_circ_0000345 expression was manipulated (overexpression and down-regulation).
- Cell viability (MTT assay), apoptosis (flow cytometry), cell cycle, invasion (Transwell assay), and HIF-1α expression were assessed.
Main Results:
- Ox-LDL treatment significantly decreased hsa_circ_0000345 expression in ASMCs.
- Overexpression of hsa_circ_0000345 enhanced cell viability and inhibited apoptosis.
- Down-regulation of hsa_circ_0000345 reduced cell viability and promoted apoptosis.
- hsa_circ_0000345 overexpression arrested cell cycle at G1 phase and enhanced invasion in ox-LDL treated ASMCs.
- hsa_circ_0000345 regulated HIF-1α expression at both mRNA and protein levels.
Conclusions:
- hsa_circ_0000345 acts as a crucial regulator of ASMC proliferation, apoptosis, and invasion under ox-LDL conditions.
- hsa_circ_0000345 demonstrates a protective role against ox-LDL-induced cellular damage in ASMCs.
- These findings highlight hsa_circ_0000345 as a potential therapeutic target for atherosclerosis.
Abstract:
The interaction between circRNAs and atherosclerosis has been extensively studied. However, more novel circRNAs need to be explored to help establish a perfect regulatory network. In the present research, hsa_circ_0000345 was demonstrated to regulate cellular development of oxygenized low-density lipoprotein (ox-LDL)-treated aortic smooth muscle cells (ASMCs), which was closely related to the occurrence and progress of atherosclerosis. Ox-LDL exposure remarkably decreased hsa_circ_0000345 expression in ASMCs. Transfection-induced hsa_circ_0000345 overexpression activated cell viability (detected by an MTT assay) and restrained cellular apoptosis (analysed by flow cytometry) in the atherosclerosis cellular model. While down-regulation of hsa_circ_0000345 reduced cell viability and promoted cell apoptosis. In addition, the data of the cell cycle distribution analysis and trans-well assay indicated that cell cycle progression was arrested at the G1 phase while cell invasion was enhanced in ASMCs following treatment of ox-LDL in the context of hsa_circ_0000345 OE plasmids. In addition, up-regulation of hsa_circ_0000345 supported HIF-1α at both the mRNA and protein level, and down-regulation of hsa_circ_0000345 reduced HIF-1α expression. Overall, the above findings revealed that hsa_circ_0000345 was a dramatic regulator of ASMCs proliferation, apoptosis and invasion in response to ox-LDL treatment. Hsa_circ_0000345 was identified as a protector of cell viability during ox-LDL induced cell development.
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