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Updated: Feb 10, 2026

Measurement of the Compressibility of Cell and Nucleus Based on Acoustofluidic Microdevice
Published on: July 14, 2022
CsA attenuates compression-induced nucleus pulposus mesenchymal stem cells apoptosis via alleviating mitochondrial
Zhiliang Li1, Songfeng Chen2, Kaige Ma1
1Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Aims:
This study aims to investigate the protective effects and potential mechanisms of cyclosporine A (CsA), which efficiently inhibits mitochondrial permeability transition pore (MPTP) opening, on compression-induced apoptosis of human nucleus pulposus mesenchymal stem cells (NP-MSCs).
Materials And Methods:
Human NP-MSCs were subjected to various periods of 1.0 MPa compression. Cell viability was evaluated using cell counting kit-8 (CCK-8) assay. The cellular ultrastructure and ATP level were analyzed via transmission electron microscopy (TEM) and ATP detection kit respectively. The apoptosis ratio was determined using Annexin V/PI dual staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assays. The levels of apoptosis-associated molecules (cleaved caspase-3, Bax and Bcl-2) were analyzed by western blot and qRT-PCR. Additionally, MPTP opening, mitochondrial membrane potential (MMP) and the levels of oxidative stress-related indicators (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA) were monitored.
Key Findings:
Annexin V/PI dual staining and detection of apoptosis-associated molecules demonstrated that compression significantly up-regulated apoptosis level of NP-MSCs in a time-dependent manner. CsA greatly down-regulated compression-mediated NP-MSC apoptosis and the cell death ratio. Compression also notably exacerbated mitochondrial dysfunction, ATP depletion and oxidative stress in NP-MSCs, all of which were rescued by CsA.
Significance:
Our results demonstrated that CsA efficiently inhibited compression-induced NP-MSCs apoptosis by alleviating mitochondrial dysfunction and oxidative stress. These findings provide new insights into intervertebral disc (IVD) degeneration (IVDD), and suggest CsA treatment as a potential strategy for delaying or even preventing IVDD.
Insights
Cyclosporine A (CsA) protects human nucleus pulposus mesenchymal stem cells (NP-MSCs) from compression-induced apoptosis. CsA alleviates mitochondrial dysfunction and oxidative stress, offering a potential strategy for intervertebral disc degeneration (IVDD).
Area of Science:
- Biomedical Engineering
- Cell Biology
- Regenerative Medicine
Background:
- Intervertebral disc degeneration (IVDD) is a significant cause of low back pain.
- Mesenchymal stem cells (MSCs) are crucial for disc homeostasis, but are susceptible to mechanical stress.
- Compression-induced apoptosis of nucleus pulposus MSCs (NP-MSCs) contributes to IVDD.
Purpose of the Study:
- To investigate the protective effects of cyclosporine A (CsA) on NP-MSCs under compression.
- To elucidate the mechanisms by which CsA inhibits apoptosis, focusing on mitochondrial function and oxidative stress.
- To evaluate CsA as a potential therapeutic agent for IVDD.
Main Methods:
- Human NP-MSCs were subjected to mechanical compression.
- Cell viability, apoptosis ratio, and cellular ultrastructure were assessed.
- Mitochondrial function (MPTP opening, MMP, ATP levels) and oxidative stress markers (ROS, SOD, MDA) were measured.
- Apoptosis-associated molecules were analyzed via western blot and qRT-PCR.
Main Results:
- Compression significantly increased NP-MSC apoptosis in a time-dependent manner.
- CsA treatment effectively reduced compression-induced apoptosis and cell death.
- CsA rescued compression-induced mitochondrial dysfunction, ATP depletion, and oxidative stress.
Conclusions:
- CsA protects NP-MSCs from compression-induced apoptosis by mitigating mitochondrial dysfunction and oxidative stress.
- These findings highlight CsA's potential as a therapeutic strategy to delay or prevent IVDD.
- Further research into CsA's role in disc regeneration is warranted.
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