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Updated: Jan 27, 2026

Preparation and In Vitro Characterization of Magnetized miR-modified Endothelial Cells
Published on: May 2, 2017
miR-573 regulates cell proliferation and apoptosis by targeting Bax in nucleus pulposus cells
Rui Wang1, Boping Wen2, Dong Sun1
11Department of Massage and Physiotherapy, Guang Xing Hospital, Zhejiang University of Traditional Chinese Medicine, No. 453, Tiyuchang Road, Xihu District, Hangzhou, Zhejiang 310007 People's Republic of China.
Background:
MicroRNA (miRNA) plays a vital role in the pathogenesis of intervertebral disc degeneration (IDD). The expression and potential mechanism of miR-573 in human nucleus pulposus (NP) remains to be elucidated. In this study, we aimed to investigate the role of miR-573 in IDD.
Methods:
Quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis was applied to examine the expression of miR-573 and Bax in idiopathic scoliosis tissues and IDD tissues. Human NP cells were employed for analysis. Moreover, the proliferation and apoptosis of NP cells were detected using MTT and flow cytometry assay respectively. The expression levels of Bcl-2, cleaved caspase-3, cleaved caspase-9, caspase-3 and caspase-9 in degenerative NP cells were measured by Western blotting assay. Furthermore, a luciferase reporter assay was used to verify the relationship between miR-573 and Bax.
Results:
The results revealed that the mRNA expression level of miR-573 was down-regulated whereas Bax was up-regulated notably in degenerative NP cells. In addition, overexpression of miR-573 increased cell viability remarkably, coupled with inhibition of cell apoptosis. The expression level of Bcl-2 was increased while cleaved caspase-3 and cleaved caspase-9 expression levels were decreased in miR-573 overexpression NP cells. Additionally, the bioinformatics analysis underscored that Bax was a direct target gene of miR-573.
Conclusion:
These results suggest that overexpression of miR-573 inhibited NP cell apoptosis by down-regulating Bax, which proved to be a novel effective strategy for IDD therapies.
Insights
Overexpression of microRNA-573 (miR-573) inhibits nucleus pulposus cell apoptosis by down-regulating Bax, offering a potential therapeutic strategy for intervertebral disc degeneration (IDD). This study clarifies miR-573
Area of Science:
- Biochemistry
- Molecular Biology
- Cell Biology
Background:
- MicroRNAs (miRNAs) are critical in intervertebral disc degeneration (IDD) pathogenesis.
- The specific role and mechanism of miR-573 in human nucleus pulposus (NP) cells require further investigation.
- This study focuses on elucidating the function of miR-573 in IDD.
Purpose of the Study:
- To investigate the expression and function of miR-573 in human nucleus pulposus (NP) cells.
- To determine the therapeutic potential of miR-573 in intervertebral disc degeneration (IDD).
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) to assess miR-573 and Bax expression.
- MTT and flow cytometry assays to evaluate NP cell proliferation and apoptosis.
- Western blotting to measure apoptosis-related proteins (Bcl-2, caspase-3, caspase-9).
- Luciferase reporter assay to confirm the direct targeting of Bax by miR-573.
Main Results:
- miR-573 expression was significantly downregulated, while Bax expression was upregulated in degenerative NP cells.
- Overexpression of miR-573 enhanced NP cell viability and inhibited apoptosis.
- miR-573 overexpression led to increased Bcl-2 and decreased cleaved caspase-3/caspase-9 levels.
- Bax was identified as a direct target gene of miR-573.
Conclusions:
- Overexpression of miR-573 suppresses NP cell apoptosis by downregulating Bax.
- miR-573 acts as a protective factor against IDD.
- Targeting miR-573 represents a promising therapeutic strategy for IDD.
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