Acid‐sensing ion channel 1a mediates acid‐induced pyroptosis through calpain‐2/calcineurin pathway in rat articular chondrocytes

2020 ◽  
Vol 44 (10) ◽  
pp. 2140-2152 ◽  
Author(s):  
Sheng‐Qin Zu ◽  
Yu‐Bin Feng ◽  
Chuan‐Jun Zhu ◽  
Xiao‐Shan Wu ◽  
Ren‐Peng Zhou ◽  
...  
Keyword(s):  
Ion Channel ◽  
Articular Chondrocytes ◽  
Calpain 2 ◽  
Calcineurin Pathway

Acid-sensing ion channel 1a mediates acid-induced increases in intracellular calcium in rat articular chondrocytes

2010 ◽  
Vol 340 (1-2) ◽  
pp. 153-159 ◽  
Author(s):  
Feng-Lai Yuan ◽  
Fei-Hu Chen ◽  
Wei-Guo Lu ◽  
Xia Li ◽  
Fan-Rong Wu ◽  
...  
Keyword(s):  
Ion Channel ◽  
Intracellular Calcium ◽  
Articular Chondrocytes

scholarly journals A6 FUNCTIONAL CHARACTERIZATION OF TRPV4 AS AN OSMOTICALLY SENSITIVE ION CHANNEL IN ARTICULAR CHONDROCYTES

2008 ◽  
Vol 16 ◽  
pp. S15-S16 ◽  
Author(s):  
H.A. Leddy ◽  
M. Phan ◽  
B.J. Votta ◽  
S. Kumar ◽  
S. Lee ◽  
...  
Keyword(s):  
Ion Channel ◽  
Articular Chondrocytes ◽  
Functional Characterization

scholarly journals Acid-Sensing Ion Channel-1a in Articular Chondrocytes and Synovial Fibroblasts: A Novel Therapeutic Target for Rheumatoid Arthritis

2021 ◽  
Vol 11 ◽  
Author(s):  
Yayun Xu ◽  
Feihu Chen
Keyword(s):  
Rheumatoid Arthritis ◽  
Articular Cartilage ◽  
Ion Channel ◽  
Articular Chondrocytes ◽  
Distribution Channel ◽  
Bone Destruction ◽  
Synovial Fibroblasts ◽  
Synovial Inflammation ◽  
And Function ◽  
Chronic Autoimmune Disease

Acid-sensing ion channel 1a (ASIC1a) is a member of the extracellular H+-activated cation channel family. Emerging evidence has suggested that ASIC1a plays a crucial role in the pathogenesis of rheumatoid arthritis (RA). Specifically, ASIC1a could promote inflammation, synovial hyperplasia, articular cartilage, and bone destruction; these lead to the progression of RA, a chronic autoimmune disease characterized by chronic synovial inflammation and extra-articular lesions. In this review, we provided a brief overview of the molecular properties of ASIC1a, including the basic biological characteristics, tissue and cell distribution, channel blocker, and factors influencing the expression and function, and focused on the potential therapeutic targets of ASIC1a in RA and possible mechanisms of blocking ASIC1a to improve RA symptoms, such as regulation of apoptosis, autophagy, pyroptosis, and necroptosis of articular cartilage, and synovial inflammation and invasion of fibroblast-like cells in synovial tissue.

scholarly journals Functional characterization of TRPV4 as an osmotically sensitive ion channel in porcine articular chondrocytes

2009 ◽  
Vol 60 (10) ◽  
pp. 3028-3037 ◽  
Author(s):  
Mimi N. Phan ◽  
Holly A. Leddy ◽  
Bartholomew J. Votta ◽  
Sanjay Kumar ◽  
Dana S. Levy ◽  
...  
Keyword(s):  
Ion Channel ◽  
Articular Chondrocytes ◽  
Functional Characterization

Modelling the Ion Channel Behaviour of Articular Chondrocytes

2002 ◽  
Author(s):  
Jim R. Wilson ◽  
Neil A. Duncan
Keyword(s):  
Membrane Potential ◽  
Ion Channels ◽  
Patch Clamp ◽  
Ion Channel ◽  
Articular Chondrocytes ◽  
Membrane Conductance ◽  
Excitable Cells ◽  
Excitable Tissue ◽  
Tissue Cells ◽  
Opening And Closing

All cells have a membrane potential; this voltage difference arises from the different intracellular and extracellular ion concentrations. In excitable tissue the cell membranes contain ion channels which control the movement of ions and hence control the cell’s membrane potential. Extensive measurements of the electrophysiology of excitable cells has allowed considerable understanding of the ion channels. The Hodgkin-Huxley model [1] was developed from measurements on a squid nerve axon, and it quantifies the changes in membrane conductance due to the opening and closing of specific ion channels. This model has been very successful in describing the electrical behaviour of neurons. Ion channels also exist in non-excitable tissue cells. Patch clamp experiments have demonstrated that ion channels in chondrocytes influence cell’s membrane potential [2]; controls the influx of Ca2+ [3] and may regulate cell proliferation [2]. The objective of this research was to develop a model of ion channel behaviour for connective tissue cells based on the Hodgkin-Huxley model, and to apply this model to reported patch clamp measurements of articular chondrocytes.

Osmotic or Chemical Activation of the TRPV4 Ion Channel Enhances the Development of Chondrocyte-Based Tissue Engineered Cartilage

2013 ◽  
Author(s):  
Christopher J. O’Conor ◽  
Halei C. Benefield ◽  
Wolfgang Liedtke ◽  
Farshid Guilak
Keyword(s):  
Ion Channel ◽  
Mechanical Loading ◽  
Functional Properties ◽  
Articular Chondrocytes ◽  
Metabolic Response ◽  
Chemical Activation ◽  
Osmotic Loading ◽  
Novel Strategy ◽  
Engineered Cartilage ◽  
Biophysical Effects

Dynamic mechanical loading can enhance the formation of engineered cartilage, potentially through secondary biophysical effects such as changes in interstitial osmolarity. This study examined the effects of daily osmotic loading, as well as direct activation of the osmosensitive ion channel TRPV4, on the biochemical and functional properties of chondrocyte-laden cartilage constructs. Osmotic loading, as well as exposure to the TRPV4-specific agonist GSK1016790A, enhanced extracellular matrix (ECM) accumulation, and TRPV4 activation enhanced the functional properties of the constructs. This study implicates the Ca ++-permeable TRPV4 ion channel in the metabolic response of articular chondrocytes to osmotic and mechanical loading. Furthermore, these results suggest that targeting TRPV4, either directly with channel agonists, or indirectly via osmotic loading, may provide a novel strategy for enhancing tissue engineered cartilage construct maturation.

scholarly journals Interleukin-6 enhances acid-induced apoptosis via upregulating acid-sensing ion channel 1a expression and function in rat articular chondrocytes

2015 ◽  
Vol 29 (2) ◽  
pp. 748-760 ◽  
Author(s):  
Renpeng Zhou ◽  
Xiaoshan Wu ◽  
Zhisen Wang ◽  
Jinfang Ge ◽  
Feihu Chen
Keyword(s):  
Ion Channel ◽  
Interleukin 6 ◽  
Articular Chondrocytes ◽  
Induced Apoptosis ◽  
And Function
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