What question did this study set out to answer?

To evaluate whether mechanical overload injury enhances cytokine-mediated proteoglycan catabolism driven by TNF-α and IL-6/sIL-6R in articular cartilage.

September 29, 2009Arthritis & Rheumatism

Mechanical injury potentiates proteoglycan catabolism induced by interleukin‐6 with soluble interleukin‐6 receptor and tumor necrosis factor α in immature bovine and adult human articular cartilage

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To evaluate whether mechanical overload injury enhances cytokine-mediated proteoglycan catabolism driven by TNF-α and IL-6/sIL-6R in articular cartilage.
Subjected immature bovine and adult human articular cartilage explants to mechanical overload injury.
Cultured injured and uninjured cartilage tissues with TNF-α, IL-6 with soluble IL-6 receptor (sIL-6R), and an IL-6-blocking Fab fragment to quantify glycosaminoglycan (GAG) loss and spatial degradation patterns.
Mechanical injury potentiated the catabolic breakdown of proteoglycans induced by both TNF-α and IL-6/sIL-6R in bovine and human cartilage tissue.
Glycosaminoglycan loss driven by mechanical injury combined with TNF-α was partially abrogated by the IL-6-blocking Fab, demonstrating that catabolic effects depend in part on endogenous IL-6.
The spatial and temporal progression of tissue breakdown indicated that overload injury alters the transport of degradative biomolecules through the cartilage matrix.

Implication

Laboratory study reveals mechanical injury accelerates cytokine-induced proteoglycan degradation in human and bovine cartilage, highlighting the synergistic role of physical overload and inflammation.

Abstract

Our findings indicate that mechanical injury potentiates the catabolic effects of TNFalpha and IL-6/sIL-6R in causing proteoglycan degradation in human and bovine cartilage. The temporal and spatial evolution of degradation suggests the importance of transport of biomolecules, which may be altered by overload injury. The catabolic effects of injury plus TNFalpha appeared partly due to endogenous IL-6, since GAG loss was partially abrogated by an IL-6-blocking Fab.

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Cite This Study

Sui et al. (2009) studied this question.

synapsesocial.com/papers/69def9355e217d93a55591fb https://doi.org/10.1002/art.24857

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Mechanical injury potentiates proteoglycan catabolism induced by interleukin‐6 with soluble interleukin‐6 receptor and tumor necrosis factor α in immature bovine and adult human articular cartilage

Key Points

Implication

Abstract

Discussion

Cite This Study

Mechanical injury potentiates proteoglycan catabolism induced by interleukin‐6 with soluble interleukin‐6 receptor and tumor necrosis factor α in immature bovine and adult human articular cartilage

Key Points

Implication

Abstract

Discussion

Cite This Study

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