Expression of superficial zone protein in mandibular condyle cartilage

Ohno, Shigeru; Schmid, Thomas; Tanne, Yuki; Kamiya, Takashi; Honda, K.; Ohno-Nakahara, M.; Swentko, N.; Desai, Tejal A.; Tanne, Kazuo; Knudson, Cheryl B.; Knudson, Warren

doi:10.1016/j.joca.2006.02.002

Cited by 35 publications

(40 citation statements)

References 36 publications

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“…This study provides new insight into the functional consequences of cytokine-mediated changes in lubricin metabolism reported previously (11,(27)(28)(29)(30)(31)(32). Changes in boundary mode eq (Figure 4) corresponded to previously demonstrated changes in lubricin localization induced by TGF␤1, IL-1␤, and OSM (27).…”

Section: Discussionsupporting

confidence: 84%

“…Bovine cartilage explants exposed in vitro to transforming growth factor ␤1 (TGF␤1) demonstrate an up-regulation of lubricin synthesis and surface localization (11,(27)(28)(29)(30)(31). In addition, TGF␤1 is known to mediate lubricin expression, which colocalizes to areas of low friction coefficient within the joint (32), while insulin-like growth factor 1, another potent anabolic signaling molecule in cartilage, does not affect lubricin metabolism and localization (28).…”

mentioning

confidence: 99%

“…In addition, TGF␤1 is known to mediate lubricin expression, which colocalizes to areas of low friction coefficient within the joint (32), while insulin-like growth factor 1, another potent anabolic signaling molecule in cartilage, does not affect lubricin metabolism and localization (28). Conversely, bovine explants treated with typical catabolic soluble factors, such as interleukin-1␣ (IL-1␣) (28), IL-1␤ (11,27,30), and tumor necrosis factor ␣ (TNF␣) (27,31), demonstrate a down-regulation of lubricin synthesis and tissue surface localization. IL-1␤ and TNF␣ have been found to be up-regulated in patients with unilateral anterior cruciate ligament injury (33) and in a rat model of antigen-induced arthritis (26), while lubricin expression is down-regulated and the friction coefficient is increased.…”

mentioning

confidence: 99%

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Alteration of articular cartilage frictional properties by transforming growth factor β, interleukin‐1β, and oncostatin M

Gleghorn¹,

Jones²,

Flannery³

et al. 2009

Arthritis & Rheumatism

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Objective. To evaluate the functional effects of transforming growth factor ␤1 (TGF␤1), interleukin-1␤ (IL-1␤), and oncostatin M (OSM) on the frictional properties of articular cartilage and to determine the role of cytokine-mediated changes in cartilage frictional properties by extracting and redepositing lubricin on the surface of cartilage explants.Methods. Neonatal bovine cartilage explants were cultured in the presence or absence of 10 ng/ml of TGF␤1, IL-1␤, or OSM over 48 hours. Boundary lubrication tests were conducted to determine the effects of endogenously produced surface localized lubricin and of exogenous lubricin at the tissue surface and in the lubricant solution. The initial friction coefficient ( 0 ), equilibrium friction coefficient ( eq ), and Young's modulus (E Y ) were determined from the temporal load data.Results. IL-1␤ and OSM decreased tissue glycosaminoglycan (GAG) content by ϳ20% over 48 hours and decreased E Y to a similar extent (11-17%), but TGF␤ did not alter GAG content or E Y . Alterations in proteoglycan content corresponded to changes in 0 , but endogenous lubricin decreased boundary mode eq . The addition of exogenous lubricin, either localized at the tissue surface or in the lubricating solution, did not modulate 0 , but it did lower eq in cytokine-treated cartilage.Conclusion. This study provides new insight into the functional consequences of cytokine-mediated changes in friction coefficient. In combination with established pathways of cytokine-mediated lubricin metabolism, these data provide evidence of distinct biochemical origins of boundary and biphasic pressuremediated lubrication mechanisms in cartilage, with boundary lubrication regulated by surface accumulation of lubricants and biphasic lubrication controlled by factors such as GAG content that affect water movement through the tissue.

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Section: Discussionsupporting

confidence: 84%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Alteration of articular cartilage frictional properties by transforming growth factor β, interleukin‐1β, and oncostatin M

Gleghorn¹,

Jones²,

Flannery³

et al. 2009

Arthritis & Rheumatism

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“…Concentrations of TGF-b1 and IL-1b were chosen based on previous changes in SZP protein expression in culture. 19,20 A decrease in SZP protein expression has been observed for IL-1a treatment of articular cartilage 7,21,22 and for IL-1b in mandibular condyle chondrocytes 23 at similar concentrations.…”

Section: Tissue Acquisition and Culturementioning

confidence: 71%

Regulation of the friction coefficient of articular cartilage by TGF‐β1 and IL‐1β

DuRaine

Neu

Chan

et al. 2008

Journal Orthopaedic Research

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Articular cartilage functions to provide a low-friction surface for joint movement for many decades of life. Superficial zone protein (SZP) is a glycoprotein secreted by chondrocytes in the superficial layer of articular cartilage that contributes to effective boundary lubrication. In both cell and explant cultures, TGF-b1 and IL-1b have been demonstrated to, respectively, upregulate and downregulate SZP protein levels. It was hypothesized that the friction coefficient of articular cartilage could also be modulated by these cytokines through SZP regulation. The friction coefficient between cartilage explants (both untreated and treated with TGF-b1 or IL-1b) and a smooth glass surface due to sliding in the boundary lubrication regime was measured with a pin-on-disk tribometer. SZP was quantified using an enzyme-linked immunosorbant assay and localized by immunohistochemistry. Both TGF-b1 and IL-1b treatments resulted in the decrease of the friction coefficient of articular cartilage in a location-and time-dependent manner. Changes in the friction coefficient due to the TGF-b1 treatment corresponded to increased depth of SZP staining within the superficial zone, while friction coefficient changes due to the IL-1b treatment were independent of SZP depth of staining. However, the changes induced by the IL-1b treatment corresponded to changes in surface roughness, determined from the analysis of surface images obtained with an atomic force microscope. These findings demonstrate that the low friction of articular cartilage can be modified by TGF-b1 and IL-1b treatment and that the friction coefficient depends on multiple factors, including SZP localization and surface roughness. ß

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“…Flannery et al (8) found that SZP accumulation by superficial zone chondrocytes from bovine articular cartilage was enhanced by TGF␤. Ohno and colleagues (27) reported that the expression and accumulation of SZP by fibroblasts derived from the fibrous zone of mandibular condyle cartilage was enhanced by TGF␤. In our laboratory, Khalafi et al (26) demonstrated that SZP accumulation was enhanced by BMP-7 in both explant cultures of superficial articular cartilage and monolayer cultures of superficial zone chondrocytes from bovine articular cartilage.…”

Section: Bmp Was Stronger Than That Of Superficial Zone Chondrocytesmentioning

confidence: 99%

Differential regulation of lubricin/superficial zone protein by transforming growth factor β/bone morphogenetic protein superfamily members in articular chondrocytes and synoviocytes

Niikura¹,

Reddi²

2007

Arthritis & Rheumatism

107

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Objective. To investigate the role of transforming growth factor ␤ (TGF␤)/bone morphogenetic protein (BMP) superfamily members on accumulation of superficial zone protein (SZP) in articular chondrocytes and synoviocytes.Methods. Chondrocytes and synoviocytes were isolated from articular cartilage and synovium from calf stifle joints and cultured as monolayers in serum-free chemically defined medium. Articular chondrocytes were isolated from 3 distinct zones of the cartilage: superficial, middle, and deep. Accumulation of SZP in the culture medium in response to various members of the TGF␤/BMP superfamily was demonstrated by immunoblotting and quantified by enzyme-linked immunosorbent assay.Results. TGF␤ stimulated SZP accumulation in both superficial zone chondrocytes and synoviocytes. The 3 isoforms of TGF␤ elicited a similar dose response. Inhibition of TGF␤ receptor type I kinase by the specific inhibitor SB431542 abolished the TGF␤-stimulated accumulation of SZP. BMPs up-regulated SZP accumulation in the superficial zone; however, the magnitude of the effects was not as great as was observed with TGF␤. There was an additive action between TGF␤ and BMP on SZP accumulation. The response of synoviocytes to BMP was stronger than that of superficial zone chondrocytes. Activin up-regulated SZP accumulation in synoviocytes, but not in chondrocytes.Conclusion. TGF␤ is a critical regulator of SZP accumulation in both superficial zone articular chondrocytes and synoviocytes. TGF␤ and BMP have an additive effect. Synoviocytes are more sensitive to BMP family members and activins than are superficial zone articular chondrocytes. Thus, regulation of SZP accumulation by TGF␤ /BMP superfamily members is regulated differently in articular chondrocytes and synoviocytes.

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Expression of superficial zone protein in mandibular condyle cartilage

Abstract: These results suggest that SZP plays an important role in boundary lubrication of mandible condylar cartilage, is synthesized locally within the condyle itself, and exhibits differential regulation by cell mediators relevant to mandibular condyle repairing and pathologies.

Cited by 35 publications

References 36 publications

Alteration of articular cartilage frictional properties by transforming growth factor β, interleukin‐1β, and oncostatin M

Alteration of articular cartilage frictional properties by transforming growth factor β, interleukin‐1β, and oncostatin M

Regulation of the friction coefficient of articular cartilage by TGF‐β1 and IL‐1β

Differential regulation of lubricin/superficial zone protein by transforming growth factor β/bone morphogenetic protein superfamily members in articular chondrocytes and synoviocytes

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