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A 3D System for Culturing Human Articular Chondrocytes in Synovial Fluid
09:58

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Published on: January 31, 2012

Cell volume regulation in chondrocytes.

Rebecca Lewis1, Claire H Feetham, Richard Barrett-Jolley

  • 1Department of Musculoskeletal Biology, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, UK.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|December 20, 2011
PubMed
Summary

Chondrocyte volume regulation is crucial for cartilage health, involving mechanisms like TRPV4 for volume decrease and co-transporters for volume increase. Its role in osteoarthritis requires further investigation.

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Area of Science:

  • Biomedical Engineering
  • Cell Biology
  • Biochemistry

Background:

  • Chondrocytes maintain cartilage extracellular matrix; their volume regulation is vital in physiological and pathological conditions.
  • Changes in chondrocyte volume occur during changing osmolarity, compressive loads, osteoarthritis, and endochondral ossification.
  • Regulatory volume decrease (RVD) and regulatory volume increase (RVI) are observed in articular chondrocytes, impacting cell function.

Purpose of the Study:

  • To review the identified mechanisms of regulatory volume decrease (RVD) and regulatory volume increase (RVI) in articular chondrocytes.
  • To highlight the central role of TRPV4 in RVD and the Na(+)-K(+)-2Cl(-) co-transporter in RVI.
  • To discuss the clinical significance and the relationship between chondrocyte volume regulation and cartilage damage, particularly in osteoarthritis.

Main Methods:

  • Review of existing literature on chondrocyte volume regulation mechanisms.
  • Analysis of evidence implicating specific ion channels and transporters in RVD and RVI.
  • Examination of transcriptomic changes in osteoarthritic cartilage related to volume control.

Main Results:

  • TRPV4 is strongly suggested as central to the RVD pathway in chondrocytes, though other pathway components remain unidentified.
  • RVI in articular chondrocytes appears less robust, with the Na(+)-K(+)-2Cl(-) co-transporter being a primary focus of study.
  • Transcript abundances of several ion channels involved in volume control are altered in chondrocytes from osteoarthritic cartilage.

Conclusions:

  • While TRPV4 is key for RVD, further research is needed to fully elucidate the RVD pathway.
  • RVI mechanisms in chondrocytes require more extensive investigation.
  • The precise role of chondrocyte volume regulation disturbances in the pathogenesis or consequence of cartilage damage, especially osteoarthritis, remains a critical unanswered question.