IL-10 reduces apoptosis and extracellular matrix degradation after injurious compression of mature articular cartilage

Behrendt, Peter; Preusse-Prange, A.; Klüter, T.; Haake, Markus; Rolauffs, Bernd; Grodzinsky, Alan J.; Lippross, Sebastian; Kurz, Bodo

doi:10.1016/j.joca.2016.06.016

Cited by 49 publications

(48 citation statements)

References 43 publications

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“…Many differences between OA and PTOA are known; we refer to the PTOA literature [234,235]. The here discussed data have not been derived from studies that had PTOA in mind; e.g., models of mechanical overload such as those described in [236,237], or studied therapeutic options after AC injury [238,239,240]. Thus, it remains unclear whether the here derived insights are valid under conditions known to lead to PTOA and designated studies using standardized injury models are needed.…”

Section: Discussionmentioning

confidence: 99%

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Boehme,

Rolauffs

2018

IJMS

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Osteoarthritis (OA) is a degenerative whole joint disease, for which no preventative or therapeutic biological interventions are available. This is likely due to the fact that OA pathogenesis includes several signaling pathways, whose interactions remain unclear, especially at disease onset. Early OA is characterized by three key events: a rarely considered early phase of proliferation of cartilage-resident cells, in contrast to well-established increased synthesis, and degradation of extracellular matrix components and inflammation, associated with OA progression. We focused on the question, which of these key events are regulated by growth factors, inflammatory cytokines, and/or miRNA abundance. Collectively, we elucidated a specific sequence of the OA key events that are described best as a very early phase of proliferation of human articular cartilage (AC) cells and concomitant anabolic/catabolic effects that are accompanied by incipient pro-inflammatory effects. Many of the reviewed factors appeared able to induce one or two key events. Only one factor, fibroblast growth factor 2 (FGF2), is capable of concomitantly inducing all key events. Moreover, AC cell proliferation cannot be induced and, in fact, is suppressed by inflammatory signaling, suggesting that inflammatory signaling cannot be the sole inductor of all early OA key events, especially at disease onset.

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Section: Discussionmentioning

confidence: 99%

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Boehme,

Rolauffs

2018

IJMS

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“…For applying compressive overload, an incubator‐housed loading device capable of axial compression was used similar to previous studies (Behrendt et al, ; Rolauffs et al, ). When placing the specimens into the loading chamber, their individual thickness was measured by applying a slow compression 20 μm/s ramp speed with a manual compression interrupt when a sudden increase in offset load was noted that indicated contact between platen and disk.…”

Section: Methodsmentioning

confidence: 99%

Chondrocyte death after mechanically overloading degenerated human intervertebral disk explants is associated with a structurally impaired pericellular matrix

Hofmann

Steidle

Danalache

et al. 2018

J Tissue Eng Regen Med

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A type VI collagen-rich pericellular matrix (PCM) encloses both intervertebral disk (IVD) and articular cartilage chondrocytes. In the latter, the PCM protects the chondrocytes from mechanical overload, whereas tissue degeneration is associated with PCM destruction. As little is known about the IVD PCM, we investigated chondrocyte survival after mechanical overload as well as PCM structural integrity as a function of clinical tissue degeneration. The hypothesis was that IVD degeneration may affect PCM integrity and overload-related chondrocyte survival. Cylindrical human IVD explants from patients undergoing surgical procedures for lumbar disk degeneration, disk prolapse, or spinal trauma were generated and scored. Mechanical overload was applied by single uniaxial 50% compression followed by immediate release, and the explants were live-dead stained (n = 20 explants). Type VI collagen, the major PCM component, was fluorescent stained and the extent was determined, in which individual cells were enclosed by a recognizable PCM; this was termed PCM fraction. More than 50% of chondrocytes in all degenerative IVD explants displayed <25% PCM fraction and a lower PCM fraction correlated with higher cell numbers (p < 0.001), suggesting a PCM structural impairment in IVD degeneration that is associated with chondrocyte clustering. Mechanical overload-induced significantly increased cell death (p = 0.005), and the PCM fraction was significantly lower in overload-induced cell death than in live cells (p = 0.042), suggesting that a fully present PCM has a protective role in mechanical overload. Collectively, human IVD degeneration is associated with a structural impairment of the PCM, which may promote cell death under mechanical overload.

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“…Among these enzymes, MMP‐13 predominantly cleaves COL II . ADAMTS5 is responsible for proteoglycans degradation, and NOS2 induced NO production which attribute to apoptosis of chondrocytes . Our results showed that FS of S. aureus induced expression of ADAMTS5, NOS2, MMP3, MMP13 in mature differentiated chondrocytes at passage2.…”

Section: Discussionmentioning

confidence: 61%

Exposure to fermentation supernatant of Staphylococcus aureus accelerated dedifferentiation of chondrocytes and production of antimicrobial peptides

Zhang

Sun

et al. 2017

Journal Orthopaedic Research

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Staphylococcus aureus (S. aureus) is the most popular pathogen found in septic arthritis. Despite bacteria was eradicated from joint cavity during acute infection, destruction of articular cartilage often continues for years, leading to permanent joint damage. The mechanism responsible for this consistent catabolic reaction in septic arthritis remains unclear. Here, we found that fermentation supernatant (FS) of S. aureus accelerated dedifferentiation of chondrocytes and induced expression of catabolic factors including A Disintegrin-like and Metalloproteinase with Thrombospondin-1 motifs 5, NO synthase 2, matrix metalloproteinase-3, -13. In response to FS of S. aureus stimulation, expression of antimicrobial peptides (AMPs) including β-defensin-1, -2, -3, -4, cathelicidin antimicrobial peptide (CAMP) in dedifferentiated chondrocytes was significantly higher than that in chondrocytes which maintained their differentiated phenotype. Among AMPs detected, expression of CAMP in dedifferentiated chondrocytes was observed to increase 170 times higher than that in differentiated ones. When exposed to FS of S. aureus, expression of interleukin (IL)-1β, IL-17F, and IL-22 were remarkably increased in dedifferentiated chondrocytes. These results indicated that dedifferentiation of chondrocytes caused by exposure to S. aureus might be responsible for secondary osteoarthritis (OA) after acute S. aureus infection in joint. While, one potential benefit of dedifferentiation resulted from S. aureus exposure is that chondrocytes initiates a self-protective responsiveness by producing more AMPs against bacterial infection. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:443-451, 2018.

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IL-10 reduces apoptosis and extracellular matrix degradation after injurious compression of mature articular cartilage

Cited by 49 publications

References 43 publications

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Chondrocyte death after mechanically overloading degenerated human intervertebral disk explants is associated with a structurally impaired pericellular matrix

Exposure to fermentation supernatant of Staphylococcus aureus accelerated dedifferentiation of chondrocytes and production of antimicrobial peptides

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