التفاصيل البيبلوغرافية
| العنوان: |
Transient receptor potential ankyrin 1 (trpa1) mediates il-1β-induced apoptosis in rat chondrocytes via calcium overload and mitochondrial dysfunction |
| المؤلفون: |
Songjiang Yin, Li Zhang, Liang Ding, Zhengquan Huang, Bo Xu, XiaoChen Li, Peimin Wang, Jun Mao |
| المصدر: |
Journal of Inflammation, Vol 15, Iss 1, Pp 1-9 (2018) |
| بيانات النشر: |
BMC, 2018. |
| سنة النشر: |
2018 |
| المجموعة: |
LCC:Therapeutics. Pharmacology |
| مصطلحات موضوعية: |
Chondrocyte apoptosis, Osteoarthritis, Transient receptor potential ankyrin 1, Calcium overload, Mitochondrial dysfunction, Therapeutics. Pharmacology, RM1-950 |
| الوصف: |
Abstract Background Chondrocyte apoptosis is a central feature in the progression of osteoarthritis (OA), and would be triggered by sustained elevation of intracellular calcium ion (Ca2+), also known as a cellular second messenger. Transient receptor potential ankyrin 1 (TRPA1) is a membrane-associated cation channel, and the activation of which causes an influx of cation ions, in particularly Ca2+, into the activated cells. Therefore, we investigate the potential role of TRPA1 in mediating Ca2+ influx to promote chondrocyte apoptosis in OA. Methods The expression of TRPA1 in interleukin (IL)-1β-treated rat chondrocytes was assessed by Polymerase chain reaction (PCR) and Western blot (WB), and the functionality of TRPA1 channel by Ca2+ influx measurements. Meanwhile, the chondrocyte apoptosis in IL-1β-treated cells was measured by TUNEL assay and flow cytometry. The measurement of mitochondrial membrane potential and apoptosis-associated proteins after inhibition of TRPA1 were also performed in IL-1β-treated rat chondrocytes. Results After being induced by IL-1β, the gene and protein expression of TRPA1 was increased in the dose-dependent manner. Meanwhile, Ca2+ influx mediated by TRPA1 in rat chondrocytes was also enhanced. Pharmacological inhibition of TRPA1 downregulated the apoptotic rate in IL-1β-treated rat chondrocytes. In addition, the membrane potential depolarization was improved and significantly increased expression of apoptosis-associated proteins also reduced by the TRPA1 antagonist. Conclusions We found the IL-1β caused the increased functional expression of TRPA1, the activation of which involved IL-1β-induced apoptosis in rat chondrocytes. The potential mechanism may be linked to the intracellular calcium overload mediated by TRPA1 and attendant mitochondrial dysfunction. |
| نوع الوثيقة: |
article |
| وصف الملف: |
electronic resource |
| اللغة: |
English |
| تدمد: |
1476-9255 |
| Relation: |
http://link.springer.com/article/10.1186/s12950-018-0204-9; https://doaj.org/toc/1476-9255 |
| DOI: |
10.1186/s12950-018-0204-9 |
| URL الوصول: |
https://doaj.org/article/664dc6f5515845cf92dfb7a5ee25910a |
| رقم الانضمام: |
edsdoj.664dc6f5515845cf92dfb7a5ee25910a |
| قاعدة البيانات: |
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