Dexamethasone-induced expression of the glucocorticoid response gene lipocalin 2 in chondrocytes

Owen, Heather; Roberts, Scott J.; Ahmed, S. Faisal; Farquharson, Colin

doi:10.1152/ajpendo.00586.2007

Cited by 64 publications

(63 citation statements)

References 72 publications

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“…Also known as neutrophil gelatinase-associated lipocalin (NGAL), Lcn2 is now recognized as an adipokine as it is predominantly produced by white adipose tissue [19]. Lcn2 has recently been identified in growth plate chondrocytes [20] where expression is modulated by IL-1b, leptin, adiponectin, lipopolysaccharides, and dexamethasone. The function of Lcn2 in cartilage and IVD tissue is currently unknown.…”

Section: Discussionmentioning

confidence: 99%

Nerve growth factor increases MMP9 activity in annulus fibrosus cells by upregulating lipocalin 2 expression

et al. 2014

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Purpose Nerve growth factor (NGF) expression and activity is important in chronic lower back pain but may also act as a pro-catabolic factor in the pathogenesis of intervertebral disc (IVD) degeneration. Lipocalin 2 (Lcn2) expression in IVD was upregulated by NGF stimulation in our previous study. The current study was undertaken to identify potential mechanisms of the latter effect including potential interactions between Lcn2 and matrix metalloproteinase 9 (MMP9). Methods Rat annulus fibrosus (AF) cells were stimulated by NGF and subjected to microarray analysis, subsequent real-time PCR, western immunoblotting, and immunofluorescence. Cells were treated with NGF in the absence or presence of the NGF inhibitor Ro 08-2750. Zymography and functional MMP9 assays were used to determine MMP9 activity, whilst the dimethyl-methylene blue assay was used to quantify the release of glycosaminoglycans (GAGs) reflecting catabolic effects following NGF treatment. Immunoprecipitation with immunoblotting was used to identify interactions between MMP9 and Lcn2. Results Increased expression of Lcn2 gene and protein following NGF stimulation was confirmed by microarray analysis, real-time PCR, western blot and immunofluorescence. Zymography showed that NGF enhanced 125-kDa gelatinase activity, identified as a Lcn2/MMP9 complex by immunoprecipitation and immunoblotting. Functional assays showed increased MMP9 activity and GAG release in the presence of NGF. The effects of NGF were neutralized by the presence of Ro 08-2750. Conclusions NGF upregulates Lcn2 expression and increases MMP9 activity in AF cells; processes which are likely to potentiate degeneration of AF tissue in vivo. Anti-NGF treatment may have benefit for management of pain Electronic supplementary material The online version of this article

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Section: Discussionmentioning

confidence: 99%

Nerve growth factor increases MMP9 activity in annulus fibrosus cells by upregulating lipocalin 2 expression

et al. 2014

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“…The influence of GCs has been rarely reported on chondrocytes, which play a key role in skeletal development. Sporadic studies have reported GC effects on the apoptosis and differentiation of chondrocytes (7,8). Autophagy is a lysosomal degradation process that is essential for cell growth, survival, differentiation, development and homeostasis (9).…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone reduces ATDC5 chondrocyte cell viability by inducing autophagy

Zhao

Zuo

Huo

et al. 2014

Molecular Medicine Reports

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Abstract. Prolonged use of glucocorticoids (GCs) for the treatment of chronic inflammatory and autoimmune diseases commonly exerts various side-effects, including impairment of skeletal development. However, the effect of GCs on chondrocytes, which play a key role in skeletal development, has been rarely reported. In the present study, autophagy was induced in the ATDC5 chondrocyte cell line following treatment with dexamethasone (Dex) at doses of 1-100 µM, and that this effect can be inhibited by RU486, a GC antagonist. Autophagy induced by the highest Dex dose (100 µM) was associated with a reduction in ATDC5 cell viability. We conclude that high doses of GC can reduce ATDC5 chondrocyte cell viability by inducing autophagy.

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“…LCN2 has recently been identified in chondrocytes (Owen et al, 2008). In these cells IL-1 , leptin, adiponectin, LPS and dexamethasone act as potent modulators of LCN2 expression (Conde et al, 2011).…”

Section: Lipocalinmentioning

confidence: 99%

Adipokines and Systemic Rheumatic Diseases: Linking Inflammation, Immunity and Metabolism

Scotece¹,

Conde²,

López³

et al. 2012

Insights and Perspectives in Rheumatology

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Dexamethasone-induced expression of the glucocorticoid response gene lipocalin 2 in chondrocytes

Cited by 64 publications

References 72 publications

Nerve growth factor increases MMP9 activity in annulus fibrosus cells by upregulating lipocalin 2 expression

Nerve growth factor increases MMP9 activity in annulus fibrosus cells by upregulating lipocalin 2 expression

Dexamethasone reduces ATDC5 chondrocyte cell viability by inducing autophagy

Adipokines and Systemic Rheumatic Diseases: Linking Inflammation, Immunity and Metabolism

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