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Homeostasis of intracellular Ca2+ in equine chondrocytes: response to hypotonic shock.
Abstract: Ca2+ homeostasis in articular chondrocytes affects synthesis and degradation of the cartilage matrix, as well as other cellular functions, thereby contributing to joint integrity. Although it will be affected by mechanical loading, the sensitivity of intracellular Ca2+ concentration ([Ca2+]i) in equine articular chondrocytes to many stimuli remains unknown. Objective: An improved understanding of Ca2+ homeostasis in equine articular chondrocytes, and how it is altered during joint loading and pathology, will be important in understanding how joints respond to mechanical loads. Methods: [Ca2+]i was determined using the fluorophore fura-2. We examined the effects of hypotonic shock, a perturbation experienced in vivo during mechanical loading cycles. We used inhibitors of Ca2+ transporters to ascertain the important factors in Ca2+ homeostasis. Results: Under isotonic conditions, [Ca2+]i was 148 +/- 23 nmol/l, increasing by 216 +/- 66 nmol/l in response to reduction in extracellular osmolality of 50%. Resting [Ca2+]i, and the increase following hypotonic shock, were decreased by Ca2+ removal; they were both elevated when extracellular [Ca2+] ([Ca2+]o) was raised or following Na+ removal. The hypotonicity-induced rise in [Ca2+]i was inhibited by exposure of cells to gadolinium (Gd3+; 10 micromol/l), an inhibitor of mechanosensitive channels. [Ca2+]i was also elevated following treatment of cells with thapsigargin (10 micromol/l), an inhibitor of the Ca2+ pump of intracellular stores. Conclusions: A model is presented which interprets these findings in relation to Ca2+ homeostasis in equine articular chondrocytes, including the presence of mechanosensitive channels allowing Ca2+ entry, a Na+/Ca2+ exchanger for removal of intracellular Ca2+ and intracellular stores sensitive to thapsigargin. Conclusions: A more complete understanding of Ca2+ homeostasis in equine chondrocytes may allow development of future therapeutic regimes to ameliorate joint disease.
Publication Date: 2003-07-24 PubMed ID: 12875320DOI: 10.2746/042516403775600541Google Scholar: Lookup The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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This research work is devoted to understanding how calcium homeostasis in horse cartilage cells or ‘equine chondrocytes’ responds to specific stimuli and influences the integrity of joints. Focusing on the mechanisms and potential treatments for joint diseases, the study investigates how the cells react to stress such as hypotonic shock.
Research Methodology
- The experiment largely banked on the use of fura-2, a chemical compound that glows when bound to calcium ions and thereby helping to gauge the intracellular calcium concentration ([Ca2+]i).
- The study primarily sought to determine how equine chondrocytes react to hypotonic shock, which refers to a sudden drop in the extracellular osmolality or solute concentration surrounding the cells. This type of stress occurs during mechanical loading cycles in living organisms.
- To identify key factors in calcium homeostasis, the researchers applied various inhibitors that block specific transporters responsible for calcium movement across the cell membrane.
Findings and Conclusion
- Under normal conditions (isotonic), the intracellular calcium concentration was found to be 148 +/- 23 nmol/l. However, when subjected to hypotonic shock — a 50% reduction in extracellular osmolality, the levels rose to 216 +/- 66 nmol/l.
- The resting intracellular calcium levels and its rise post-hypotonic shock were both affected by the presence of extracellular calcium. In the absence of calcium or sodium, these levels were substantially elevated.
- The rise in intracellular calcium levels induced by hypotonicity was hampered by the use of gadolinium (Gd3+), a substance that inhibits mechanosensitive channels responsible for calcium entry into the cells.
- It was also found that application of thapsigargin, a substance that inhibits the action of calcium pumps in intracellular stores, led to an increase in calcium levels.
- Based on the results, a model was proposed that included the presence of mechanosensitive channels allowing calcium entry, a sodium-calcium exchanger for removal of intracellular calcium, and intracellular stores sensitive to thapsigargin.
- In conclusion, a deeper understanding of calcium homeostasis in equine chondrocytes may pave the way for the development of therapeutic regimes to treat joint diseases.
Cite This Article
APA
Wilkins RJ, Fairfax TP, Davies ME, Muzyamba MC, Gibson JS.
(2003).
Homeostasis of intracellular Ca2+ in equine chondrocytes: response to hypotonic shock.
Equine Vet J, 35(5), 439-443.
https://doi.org/10.2746/042516403775600541 Publication
Researcher Affiliations
- University of Oxford, University Laboratory of Physiology, Parks Road, Oxford OX1 3PT, UK.
MeSH Terms
- Animals
- Calcium / metabolism
- Calcium-Transporting ATPases / antagonists & inhibitors
- Cartilage, Articular / cytology
- Cartilage, Articular / physiology
- Cells, Cultured
- Chondrocytes / metabolism
- Enzyme Inhibitors / pharmacology
- Gadolinium / pharmacology
- Homeostasis
- Horses / physiology
- Hypotonic Solutions
- Models, Biological
- Osmolar Concentration
- Thapsigargin / pharmacology
Citations
This article has been cited 5 times.- Gao W, Hasan H, Anderson DE, Lee W. The Role of Mechanically-Activated Ion Channels Piezo1, Piezo2, and TRPV4 in Chondrocyte Mechanotransduction and Mechano-Therapeutics for Osteoarthritis. Front Cell Dev Biol 2022;10:885224.
- Skiöldebrand E, Thorfve A, Björklund U, Johansson P, Wickelgren R, Lindahl A, Hansson E. Biochemical alterations in inflammatory reactive chondrocytes: evidence for intercellular network communication. Heliyon 2018 Jan;4(1):e00525.
- Hansson E, Skiöldebrand E. Coupled cell networks are target cells of inflammation, which can spread between different body organs and develop into systemic chronic inflammation. J Inflamm (Lond) 2015;12:44.
- Sánchez JC, López-Zapata DF. Effects of Adipokines and Insulin on Intracellular pH, Calcium Concentration, and Responses to Hypo-Osmolarity in Human Articular Chondrocytes from Healthy and Osteoarthritic Cartilage. Cartilage 2015 Jan;6(1):45-54.
- White R, Gibson JS. The effect of oxygen tension on calcium homeostasis in bovine articular chondrocytes. J Orthop Surg Res 2010 Apr 26;5:27.
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