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Interleukin 1 beta-induced chloride currents are important in osteoarthritis onset: an in vitro study

Authors
  • Deng, Zhiqin1
  • Lin, Zicong1
  • Zhong, Qing1
  • Lu, Minqiang1
  • Fang, Huankun1
  • Liu, Jianquan1
  • Duan, Li1
  • Chen, Lixin2
  • Wang, Liwei3, 4
  • Wang, Daping1
  • Li, Wencui1
  • 1 Guangdong Provincial Research Center for Artificial Intelligence and Digital Orthopedic Technology, Hand and Foot Surgery Department, Shenzhen Second People’s Hospital (The First Hospital Affiliated to Shenzhen University), China , (China)
  • 2 Department of Pharmacology, Medical College, Jinan University, China , (China)
  • 3 Department of Physiology, Medical College, Jinan University, China , (China)
  • 4 International School, Jinan University, China , (China)
Type
Published Article
Journal
Acta Biochimica et Biophysica Sinica
Publisher
Oxford University Press
Publication Date
Mar 02, 2021
Volume
53
Issue
4
Pages
400–409
Identifiers
DOI: 10.1093/abbs/gmab010
PMID: 33677475
PMCID: PMC7996641
Source
PubMed Central
Keywords
Disciplines
  • AcademicSubjects/SCI00980
License
Unknown

Abstract

Persistent hypotonic and inflammatory conditions in the joint cavity can lead to the loss of cartilage matrix and cell death, which are the important mechanisms of osteoarthritis (OA) onset. Previous studies have confirmed that the existence of a hypotonic environment is a red flag for inflammation, as hypotonic environment induces the opening of the chloride channel of the cell and promotes chloride ion efflux, which prompts the cell volume to increase. Chloride channels play an important role in the regulation of mineralization and chondrocyte death. Here, we reported that OA chondrocytes showed a significant increase of cell death rate and the imbalance of cartilage matrix catabolism. We found that the distribution of skeleton protein F-actin was disordered. In addition, the volume-sensitive chloride current of OA chondrocytes decreased significantly with the increase of the expression levels of inflammation-related proteins caspase-1, caspase-3, and NLRP3. Moreover, interleukin-1β (IL-1β) showed a potential to activate the chloride current of normal chondrocytes. These results indicate that IL-1β-induced chloride channel opening in chondrocytes may be closely related to the occurrence of OA. This chloride channel opening process may therefore be a potential target for the treatment of OA.

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