XCXiao-Dong Chen

Xiao-Dong Chen

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

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Xiao-Dong Chen has a total of 7 co-authors. Here are the top co-authors by number of shared publications:


Latest Publications

  • Autophagy protects meniscal cells from glucocorticoids-induced apoptosis via inositol trisphosphate receptor signaling

    by Chao Shen, Wen Gu, Gui-Quan Cai, Jian-Ping Peng, Xiao-Dong Chen

    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.


  • Efficacy of treatment in peri-pelvic Morel–Lavallee lesion: a systematic review of the literature

    by Chao Shen, Jian-Ping Peng, Xiao-Dong Chen

    Morel-Lavallee lesion (MLL) of the peri-pelvic region is less common and various treatments have been introduced to manage the lesion. No standard treatment is recommended. We performed a systematic review of literature to (1) identify the classification of peri-pelvic MLL; (2) review the treatments of the lesion and their complications; (3) define the optimal treatment of peri-pelvic MLL. A systematic search was performed via PubMed, ISI Web of Knowledge, and Embase for English abstract articles from 1966 to 2012. We identified 21 articles detailing 153 patients with peri-pelvic MLL, most of which were level IV studies. The treatments and clinical results were reviewed. For peri-pelvic MLL patients, surgical intervention was better than conservative therapy. Sclerhodesis method is attended with good outcome in the symptomatic MLL patients without fractures. Patients with peri-pelvic fractures could be managed with local suction drainage or open debridement with dead space closure technique during fracture fixation. The delayed-diagnosis cases might be treated with mass resection when fibrosis capsule was obtained in magnetic resonance imaging. Peri-pelvic MLL can be treated with various surgical methods depending on the formation of fibrosis capsule and associated injuries. Dead space closure technique is emphasized in the treatment of MLL. Higher quality of literature is required to prove this result in future research.