| Title |
Autophagy protects meniscal cells from glucocorticoids-induced apoptosis via inositol trisphosphate receptor signaling
|
|---|---|
| Published in |
Apoptosis, June 2015
|
| DOI | 10.1007/s10495-015-1146-9 |
| Pubmed ID | |
| Authors |
Chao Shen, Wen Gu, Gui-Quan Cai, Jian-Ping Peng, Xiao-Dong Chen |
| Abstract |
Intra-articular injection of glucocorticoids (GCs) has been widely used in the management of osteoarthritis and rheumatoid arthritis. Nevertheless, several studies showed that GCs had toxic effects on chondrocytes as well as synovial cells. Previously we reported the protective role of autophagy in the degeneration of meniscal tissues. However, the effects of GCs on autophagy in the meniscal cells have not been fully elucidated. To investigate whether GCs can regulate autophagy in human meniscal cells, the meniscal cells were cultured in vitro and exposed in the presence of dexamethasone. The levels of apoptosis and autophagy were investigated via flow cytometry as well as western blotting analysis. The changes of the aggrecanases were measured using real-time PCR. The role of autophagy in dexamethasone-induced apoptosis was investigated using pharmacological agents and RNA interference technique. An agonist of inositol 1,4,5-trisphosphate receptor (IP3R) was used to investigate the mechanism of dexamethasone-induced autophagy. The results showed that dexamethasone induced autophagy as well as apoptosis in normal human meniscal cells. Using RNA interference technique and pharmacological agents, our results showed that autophagy protected the meniscal cells from dexamethasone-induced apoptosis. Our results also indicated that dexamethasone increased the mRNA levels of aggrecanases. This catabolic effect of dexamethasone was enhanced by 3-MA, the autophagy inhibitor. Furthermore, our results showed that dexamethasone induced autophagy via suppressing the phosphorylation of IP3R. In summary, our results indicated that autophagy protected meniscal cells from GCs-induced apoptosis via inositol trisphosphate receptor signaling. |
X Demographics
The data shown below were collected from the profiles of 2 X users who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Germany | 1 | 50% |
| Unknown | 1 | 50% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 2 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 20 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Singapore | 1 | 5% |
| Unknown | 19 | 95% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Researcher | 9 | 45% |
| Student > Bachelor | 2 | 10% |
| Student > Master | 2 | 10% |
| Student > Ph. D. Student | 1 | 5% |
| Other | 1 | 5% |
| Other | 2 | 10% |
| Unknown | 3 | 15% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 5 | 25% |
| Biochemistry, Genetics and Molecular Biology | 3 | 15% |
| Immunology and Microbiology | 2 | 10% |
| Business, Management and Accounting | 1 | 5% |
| Veterinary Science and Veterinary Medicine | 1 | 5% |
| Other | 3 | 15% |
| Unknown | 5 | 25% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 11 August 2015.
All research outputs
#18,417,643
of 22,815,414 outputs
Outputs from Apoptosis
#550
of 806 outputs
Outputs of similar age
#189,533
of 263,898 outputs
Outputs of similar age from Apoptosis
#5
of 8 outputs
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So far Altmetric has tracked 806 research outputs from this source. They receive a mean Attention Score of 3.6. This one is in the 21st percentile – i.e., 21% of its peers scored the same or lower than it.
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