Effects of Dioxin and Estrogen on Collagenase-3 in UMR 106-01 Osteosarcoma Cells

Partridge, Nicola C.; Fiacco, Gerald J.; Walling, Hobart W.; Barmina, Olga; Jeffrey, John J.; Ruh, Mary F.

doi:10.1006/abbi.2000.1992

Cited by 13 publications

(10 citation statements)

References 30 publications

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“…Liao et al also reported that E2 caused a dose dependent decrease in MMP-1 production, with no influence on TIMP-1 expression, in osteoblast-like cells in culture. 20 Interestingly, because we show that a high concentration of E2 (10 nmol/l) maximises the expression of MMP mRNAs induced by IL1b, such a potentiality of induced MMP expression has also been shown in other cell types such as UMR 106-01 osteosarcoma cells treated with parathyroid hormone 35 and in rat fibrocartilaginous cells treated with relaxin. 34 In the classical signalling pathway, the oestrogen receptor binds to oestrogen response elements at the promoter of target genes and stimulates transcription either directly or indirectly through cofactors.…”

Section: Discussionsupporting

confidence: 63%

“…Rabbit articular chondrocytes were incubated for 20 hours and analysed for 35 23 The strips were then allowed to dry and each sample was separately cut into pieces. Scintillation liquid was added to each sample, and counted in a Packard tricarb b-spectrometer.…”

Section: Treatment Of Chondrocytes With Different Effectorsmentioning

confidence: 99%

“…The total volume (Vt) of the column was determined by the use of free [ 35 SO 4 ]sulphate. The partition coefficient (Kav) of 35 SO 4 labelled PGs in each fraction was calculated as follows:…”

Section: Chromatographymentioning

confidence: 99%

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Dual effects of 17 -oestradiol on interleukin 1 -induced proteoglycan degradation in chondrocytes

Richette¹

2004

Annals of the Rheumatic Diseases

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Objective: T o determine whether 17b-oestradiol (E2) modulates interleukin (IL) 1b-induced proteoglycan degradation in chondrocytes, and to analyse the part played by metalloproteinases (MMPs) in this process. Methods: Primary cultured rabbit articular chondrocytes were prepared and treated with 10 ng/ml IL1b combined or not with 0.1-10 nM E2. Neosynthesised proteoglycans (PGs) were evaluated after incorporation of [ 35 SO 4 ]sulphate and further analysed after chromatography on a Sepharose 2B column. Chondrocyte mRNA levels of aggrecan, MMP-1, -3, -13, and tissue inhibitor of metalloproteinase-1 (TIMP-1) were studied by northern blot. MMP-1 activity was measured by zymography. MMP-1 gene transcription was studied by transient transfection of chondrocytes with an MMP-1-luciferase construct. Results: E2 modulated the IL1b-induced total sulphated PGs in rabbit articular chondrocytes, which decreased as the E2 concentration was increased. At a low concentration (0.1 nmol/l) E2 counteracts the IL1b-induced decrease in sulphated PG, while at high concentration (10 nmol/l) E2 enhances the IL1b effects. A biphasic E2 effect was also observed on IL1b-induced disaggregation of PG, 53-58 kDa gelatinolytic activity, and MMP-1, -3, and -13 mRNA levels. In contrast, E2 did not modify the level of aggrecan mRNA and had no effect on TIMP-1 mRNA expression. Finally, simultaneous addition of IL1b and E2 (0.1-10 nmol/l) did not modify IL1b-induced MMP-1-luciferase activity, suggesting that E2 effects probably occur at the post-transcriptional level of MMP gene expression. Conclusion: Oestrogen concentration may have an inverse effect on IL1b stimulated proteoglycan degradation and MMP production by chondrocytes. O steoarthritis (OA) is the most common cause of musculoskeletal pain and disability. It is characterised by cartilage loss, subchondral sclerosis, cyst, and osteophyte formation. Although OA is a progressive and heterogeneous disorder of unknown aetiology, mechanical and genetic factors appear to have a major role.

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Section: Discussionsupporting

confidence: 63%

Section: Treatment Of Chondrocytes With Different Effectorsmentioning

confidence: 99%

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Dual effects of 17 -oestradiol on interleukin 1 -induced proteoglycan degradation in chondrocytes

Richette¹

2004

Annals of the Rheumatic Diseases

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“…E2 (10 -8 ∼10 -10 M) has similar ability to stimulate the induction of collagenase-3 mRNA in UMR 106-01 cells (Partridge et al, 2000). Transfection with either ERα or ERβ causes U2OS cell sensitivity to E2 (Lima et al, 2004;Kallio et al, 2008).…”

Section: Discussionmentioning

confidence: 93%

Transcriptional activation of insulin-like growth factor binding protein 6 by 17β-estradiol in SaOS-2 cells

et al. 2009

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Osteoblasts can synthesize the insulin-like growth factors (IGFs) and the IGF-binding proteins (IGFBPs), which may either enhance or attenuate IGF-stimulated bone cell proliferation. Since estrogen induced osteoblastic differentiation and proliferation through an estrogen-responsive gene in target cells, we investigated the effects of estrogen on IGFBP-6 expression in the human osteoblastic-like cell line SaOS-2. Expressions of IGFBP-6 protein and mRNA increased 2.8 and 2-fold, respectively, in the presence of 17-β-estradiol (E2) (0.01 to 1 μM) and estrogen receptor (ER) in SaOS-2 cells. On the other hand, E2 induced a 2-fold increase in SaOS-2 cell proliferation. To identify genomic sequences associated with estrogen responsiveness, the 5'-promoter region (-44 to +118) of the IGFBP-6 gene was cloned into a chloramphenicol acetyltransferase (CAT) reporter vector. E2 induced a 3-fold increase in CAT activity in SaOS-2 cells transiently transfected with this construct. Identification of the estrogen-responsive element (ERE) [5'-CCTTCA CCTG-3'] (-9 to +1) in this IGFBP-6 gene promoter region was confirmed using electromobility shift assays and deletion analysis. This functional ERE was important for E2-induced trans-activation of the IGFBP-6 gene.These results demonstrate that E2 exhibits a positive effect on IGFBP-6 gene transcription through estrogen-liganded ER binding to the functional ERE in the IGFBP-6 gene promoter in SaOS-2 cells.

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“…51,52) However, TCDD can positively regulate some gene expression and cell proliferation as an estrogenic-like agent. Partridge et al 53) have reported that TCDD (1 nM) and E2 (10 8-10 M) have similar abilities to stimulate the induction of collagenase-3 mRNA in UMR 106-01 cells. We believe that TCDD is not antiestrogenic at low physiological concentrations in vitro.…”

Section: Fig 7 Interaction Of Era Antibody With Igfbp-6 Gene Promotermentioning

confidence: 99%

Toxic Effects of TCDD on Osteogenesis through Altering IGFBP-6 Gene Expression in Osteoblasts

Guo

Yang

Zhao

et al. 2007

Biological & Pharmaceutical Bulletin

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Since 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has reproductive and developmental toxicity as an estrogen antagonist, we investigated the effects of TCDD on osteogenesis in rat skeleton and the human female-responsive osteoblastic osteosarcoma cell line SaOS-2. Rat fetuses were exposed to 5, 10, or 15 m mg/kg TCDD on gestation day (GD) 10. TCDD dose-dependently induced single or multiple rat fetal skeletal development malformations in vivo. In vitro, 10 nM TCDD significantly inhibited cell proliferation in the presence of 1 m mM 17-b b-estradiol (E2) in SaOS-2 cells. Insulin-like growth factor binding protein 6 (IGFBP-6), as a crucial regulator in IGF system, plays an important role in osteogenesis and bone function. TCDD (15 m mg/kg) induced a dramatic 3-fold increase in IGFBP-6 mRNA expression in rat fetal calvaria on GD 21. On the other hand, the concurrent treatment of 10 nM TCDD and 1 m mM E2 resulted in a significant increase in IGFBP-6 mRNA and protein after 24 h in SaOS-2 cells, but TCDD and (or) E2 had no effect on the mRNA level of cytosolic aromatic hydrocarbon receptor. The functional estrogen-responsive element (ERE) [5-CCT TCA CCT G-3] (؊9 to ؉1) in the IGFBP-6 promoter region was identified in this study for the first time as the ER genomic binding site. Collectively, these results suggest that TCDD can alter the expression of IGFBP-6 gene and exerts growth-inhibitory effects on osteogenesis. In addition, TCDD exhibits an anti-estrogenic effect through its interference with the binding of activated estrogen-liganded ER to the functional ERE in IGFBP-6 gene promoter.

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Effects of Dioxin and Estrogen on Collagenase-3 in UMR 106-01 Osteosarcoma Cells

Cited by 13 publications

References 30 publications

Dual effects of 17 -oestradiol on interleukin 1 -induced proteoglycan degradation in chondrocytes

Dual effects of 17 -oestradiol on interleukin 1 -induced proteoglycan degradation in chondrocytes

Transcriptional activation of insulin-like growth factor binding protein 6 by 17β-estradiol in SaOS-2 cells

Toxic Effects of TCDD on Osteogenesis through Altering IGFBP-6 Gene Expression in Osteoblasts

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