scholarly journals Retinoblastoma suppression of matrix metalloproteinase 1, but not interleukin-6, through a p38-dependent pathway in rheumatoid arthritis synovial fibroblasts

2004 ◽  
Vol 50 (1) ◽  
pp. 78-87 ◽  
Author(s):  
Kathleen Bradley ◽  
John C. Scatizzi ◽  
Stefano Fiore ◽  
Eli Shamiyeh ◽  
Alisa E. Koch ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Matrix Metalloproteinase ◽  
Interleukin 6 ◽  
Synovial Fibroblasts ◽  
Matrix Metalloproteinase 1 ◽  
Dependent Pathway

scholarly journals Ribozymes that inhibit the production of matrix metalloproteinase 1 reduce the invasiveness of rheumatoid arthritis synovial fibroblasts

2004 ◽  
Vol 50 (5) ◽  
pp. 1448-1456 ◽  
Author(s):  
Edita Rutkauskaite ◽  
Wolfgang Zacharias ◽  
Jörg Schedel ◽  
Ulf Müller-Ladner ◽  
Christian Mawrin ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Matrix Metalloproteinase ◽  
Synovial Fibroblasts ◽  
Matrix Metalloproteinase 1

scholarly journals Cloning of the gene for interstitial collagenase-3 (matrix metalloproteinase-13) from rabbit synovial fibroblasts: differential expression with collagenase-1 (matrix metalloproteinase-1)

1998 ◽  
Vol 331 (1) ◽  
pp. 341-346 ◽  
Author(s):  
Matthew P. VINCENTI ◽  
Charles I. COON ◽  
J. Andrew MENGSHOL ◽  
Sue YOCUM ◽  
Peter MITCHELL ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Matrix Metalloproteinase ◽  
Time Course ◽  
Interleukin 1 ◽  
Connective Tissue Diseases ◽  
Synovial Fibroblasts ◽  
Matrix Metalloproteinase 1 ◽  
Rabbit Gene ◽  
Factor Α ◽  
Interstitial Collagenase

Cartilage, bone and the interstitial stroma, composed largely of the interstitial collagens, types I, II and III, are remodelled by three members of the metalloproteinase (MMP) family, collagenase-1 (MMP-1), collagenase-2 (MMP-8) and collagenase-3 (MMP-13). MMP-1 and MMP-13 may contribute directly to disease progression, since they are induced in patients with rheumatoid arthritis and osteoarthritis. The study of MMP-1 and MMP-13 gene regulation in models of arthritic disease has been problematic because mice and rats, which are typically used, only possess a homologue of MMP-13. Here we show that in contrast with mice and rats, rabbits possess distinct genes homologous to human MMP-1 and MMP-13. Furthermore, rabbit MMP-13 is expressed simultaneously with MMP-1 in chondrocytes and synovial fibroblasts in response to the cytokines interleukin-1 and tumour necrosis factor-α, or the phorbol ester PMA. The time course of MMP-13 induction is more rapid and transient than that of MMP-1, suggesting that distinct mechanisms regulate the expression of these two collagenases. We have cloned the rabbit MMP-13 gene from synovial fibroblasts and demonstrated that the rabbit gene shares greater homology with human MMP-13 than does the mouse interstitial collagenase. Together with the fact that mice and rats do not possess a homologue to human MMP-1, our data suggest that the rabbit provides an appropriate model for studying the roles of interstitial collagenases in connective-tissue diseases, such as rheumatoid arthritis and osteoarthritis.

scholarly journals Interleukin-6 Released from Fibroblasts Is Essential for Up-regulation of Matrix Metalloproteinase-1 Expression by U937 Macrophages in Coculture

2009 ◽  
Vol 284 (20) ◽  
pp. 13714-13724 ◽  
Author(s):  
Kamala P. Sundararaj ◽  
Devadoss J. Samuvel ◽  
Yanchun Li ◽  
John J. Sanders ◽  
Maria F. Lopes-Virella ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Interleukin 6 ◽  
Matrix Metalloproteinase 1

scholarly journals Overexpression of Phospholipid-hydroperoxide Glutathione Peroxidase in Human Dermal Fibroblasts Abrogates UVA Irradiation-induced Expression of Interstitial Collagenase/Matrix Metalloproteinase-1 by Suppression of Phosphatidylcholine Hydroperoxide-mediated NFκB Activation and Interleukin-6 Release

2004 ◽  
Vol 279 (44) ◽  
pp. 45634-45642 ◽  
Author(s):  
Jutta Wenk ◽  
Jutta Schüller ◽  
Christina Hinrichs ◽  
Tatjana Syrovets ◽  
Ninel Azoitei ◽  
...  
Keyword(s):  
Glutathione Peroxidase ◽  
Matrix Metalloproteinase ◽  
Uv Irradiation ◽  
Interleukin 6 ◽  
Nuclear Translocation ◽  
Phospholipid Hydroperoxide Glutathione Peroxidase ◽  
Induced Expression ◽  
Uva Irradiation ◽  
Phospholipid Hydroperoxide ◽  
Matrix Metalloproteinase 1

Phospholipid-hydroperoxide glutathione peroxidase (PHGPx) exhibits high specific activity in reducing phosphatidylcholine hydroperoxides (PCOOHs) and thus may play a central role in protecting the skin against UV irradiation-triggered detrimental long term effects like cancer formation and premature skin aging. Here we addressed the role of PHGPx in the protection against UV irradiation-induced expression of matrix metalloproteinase-1 (MMP-1). For this purpose, we created human dermal fibroblast cell lines overexpressing human PHGPx. Overexpression led to a significant increase in PHGPx activity. In contrast to a maximal 4.5-fold induction of specific MMP-1 mRNA levels in vector-transfected cells at 24 h after UVA irradiation, no MMP-1 induction occurred at any studied time point after UVA treatment of PHGPx-overexpressing fibroblasts. As interleukin-6 (IL-6) was earlier shown to mediate the UVA induction of MMP-1, we studied whether PHGPx overexpression might interfere with the NFκB-mediated IL-6 induction and downstream signaling. Using transient transfections of IL-6 promoter constructs containing NFκB binding sites, we observed a high induction of the reporter gene luciferase in vector-transfected control cells and a significantly lower induction in PHGPx-overexpressing fibroblasts following UVA irradiation. Consistently both UVA irradiation and treatment of fibroblasts with PCOOHs led to phosphorylation and nuclear translocation of the p65 subunit, whereas cells overexpressing PHGPx exhibited impaired NFκB activation, p65 phosphorylation, and nuclear translocation. In line with this, the PHGPx-overexpressing fibroblasts showed a reduced constitutive and UVA irradiation-induced IL-6 release. After incubating PHGPx-overexpressing cells with PCOOHs a reduced induction of IL-6 was observed. This together with the suppression of UVA irradiation-induced IL-6 release in the presence of Trolox, a chain breaker of PCOOH-initiated lipid peroxidation, indicates that UVA irradiation-induced PCOOHs and subsequent lipid peroxides initiate the NFκB-mediated induction of IL-6, which mediates the induction of MMP-1. Our finding is particularly relevant in light of the already available small molecule mimetics of PHGPx.

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