Regulation of matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 in MCF-7 cells: comparison with regulatory mechanisms of pS2 expression

1996 ◽  
Vol 14 (4) ◽  
pp. 381-388 ◽  
Author(s):  
Anne Hansen Ree ◽  
Gunhild M. M�landsmo ◽  
�ystein Fodstad
Keyword(s):  
Matrix Metalloproteinase ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Regulatory Mechanisms ◽  
Tissue Inhibitor ◽  
Matrix Metalloproteinase 1 ◽  
Mcf 7

Pravastatin increases the expression of the tissue inhibitor of matrix metalloproteinase-1 and the oncogeneBaxin human aortic abdominal aneurysms

2008 ◽  
Vol 86 (7) ◽  
pp. 431-437 ◽  
Author(s):  
Petra J. Mateos-Cáceres ◽  
Antonio J. López-Farré ◽  
Pilar C. Morata ◽  
Priscila Ramos-Mozo ◽  
Carlos Macaya ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Apoptotic Index ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Tissue Inhibitor ◽  
Hmg Coa Reductase ◽  
Matrix Metalloproteinase 1 ◽  
Abdominal Aortic ◽  
Coa Reductase ◽  
Metalloproteinase 9

The effect of pravastatin on matrix metalloproteinase-9 (MMP-9) and the level of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 was studied in explants of human abdominal aortic aneurysm (AAA) obtained from 13 patients. The effect of pravastatin on the apoptotic status of human AAA explants was also examined. Total MMP-9 content did not differ in human AAA explants incubated in vitro in the presence or absence of pravastatin (10−6mol/L) for 48 h. TIMP-1 levels were significantly increased in pravastatin-incubated AAA explants, but TIMP-2 production was not modified by pravastatin. Western blot experiments showed that, whereas Bax expression was increased in pravastatin-incubated AAA explants, the expression of Bcl-2 was not modified. On the other hand, the ratio of the expression of Bax to Bcl-2, an apoptotic index, was not modified by pravastatin. In the human AAA explants, the increase in Bax expression, but not the increase in TIMP-1 expression elicited by pravastatin, was reversed by l-mevalonate, a downstream HMG-CoA reductase metabolite, suggesting that the expression of Bax and TIMP-1 followed HMG-CoA reductase-dependent and -independent pathways, respectively. In conclusion, pravastatin increases both TIMP-1 and Bax expression in human AAA explants without changes in either MMP-9 activity or the apoptotic status.

Matrix metalloproteinase and tissue inhibitor of metalloproteinase in serum and synovial fluid of osteoarthritic dogs

2006 ◽  
Vol 19 (01) ◽  
pp. 49-55 ◽  
Author(s):  
J. K. Roush ◽  
T. Schermerhorn ◽  
K. E. Mitchell ◽  
B. J. Salinardi
Keyword(s):  
Mass Spectrometry ◽  
Synovial Fluid ◽  
Matrix Metalloproteinase ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Matrix Metalloproteinase 2 ◽  
Tissue Inhibitor ◽  
Matrix Metalloproteinase 1 ◽  
Early Oa

SummaryTo better understand the mechanisms responsible for the pathological processes of osteoarthritis (OA) and to potentially identify a profile of changes that could be predictive of early OA, matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of matrix metalloproteinase-2 (TIMP-2) in the synovial fluid and serum of normal and osteoarthritic dogs were examined. The concentration of MMP-1 in the synovial fluid of osteoarthritic dogs (0.62 ± 0.16), as measured by densitometry, was significantly higher than that found in control dogs (0.42 ± 0.19) (P = 0.03). The concentration of MMP-1 in the serum of osteoarthritic dogs (0.74 ± 0.16) was significantly less than that found in control dogs (0.87 ± 0.08) (P = 0.05). The concentration of TIMP-2 in the synovial fluid of osteoarthritic dogs (46.2 ± 21.9 ng/ml) was significantly less than that of control dogs (122.0 ± 66.5 ng/ml) (P = 0.009). The concentration of TIMP-2 in the serum of osteoarthritic dogs (116.2 ± 43.1 ng/ml) was not significantly different than that of control dogs (95.1 ± 94.4 ng/ml) (P = 0.554). In addition, a phospho-tyrosine immunoprecipitation and mass spectrometry were used to isolate and identify interferonalpha in canine synovial fluid.

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