l-Lysine regulates tumor necrosis factor-alpha and matrix metalloproteinase-3 expression in human osteoarthritic chondrocytes

2016 ◽  
Vol 51 (7) ◽  
pp. 904-911 ◽  
Author(s):  
Teng-Le Huang ◽  
Chang-Chin Wu ◽  
Jiashing Yu ◽  
Shoichiro Sumi ◽  
Kai-Chiang Yang
Keyword(s):  
Tumor Necrosis Factor ◽  
Matrix Metalloproteinase ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Matrix Metalloproteinase 3 ◽  
Osteoarthritic Chondrocytes ◽  
Factor Alpha ◽  
Necrosis Factor

Contribution to the regulation of intestinal matrix metalloProteinase expression by tumor necrosis factor alpha in inflammatory bowel disease

2003 ◽  
Vol 124 (4) ◽  
pp. A324
Author(s):  
Martin J.W. Meijer ◽  
Wim Van Duijin ◽  
Marij A.C. Mieremet-Ooms ◽  
Annie M. Van der Zon ◽  
Qiang Gao ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Tumor Necrosis Factor ◽  
Matrix Metalloproteinase ◽  
Tumor Necrosis Factor Alpha ◽  
Bowel Disease ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Inflammatory Bowel ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals FoxO4 Regulates Tumor Necrosis Factor Alpha-Directed Smooth Muscle Cell Migration by Activating Matrix Metalloproteinase 9 Gene Transcription

2007 ◽  
Vol 27 (7) ◽  
pp. 2676-2686 ◽  
Author(s):  
Hao Li ◽  
Jianping Liang ◽  
Diego H. Castrillon ◽  
Ronald A. DePinho ◽  
Eric N. Olson ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Tumor Necrosis Factor ◽  
Matrix Metalloproteinase ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Metalloproteinase 9 ◽  
Necrosis Factor

ABSTRACT Phenotypic modulation of vascular smooth muscle cells (SMCs) in the blood vessel wall from a differentiated to a proliferative state during vascular injury and inflammation plays an important role in restenosis and atherosclerosis. Matrix metalloproteinase 9 (MMP9) is a member of the MMP family of proteases, which participate in extracellular matrix degradation and turnover. MMP9 is upregulated and required for SMC migration during the development of restenotic and atherosclerotic lesions. In this study, we show that FoxO4 activates transcription of the MMP9 gene in response to tumor necrosis factor alpha (TNF-α) signaling. Inhibition of FoxO4 expression by small interfering RNA or gene knockout reduces the abilities of SMCs to migrate in vitro and inhibit neointimal formation and MMP9 expression in vivo. We further show that both the N-terminal, Sp1-interactive domain and the C-terminal transactivation domain of FoxO4 are required for FoxO4-activated MMP9 transcription. TNF-α signaling upregulates nuclear FoxO4. Our studies place FoxO4 in the center of a transcriptional regulatory network that links gene transcription required for SMC remodeling to upstream cytokine signals and implicate FoxO4 as a potential therapeutic target for combating proliferative arterial diseases.

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