Transcription factor decoys for activator protein-1 (AP-1) inhibit oxidative stress-induced proliferation and matrix metalloproteinases in rat cardiac fibroblasts

2009 ◽  
Vol 153 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Shuanglun Xie ◽  
Ruqiong Nie ◽  
Jingfeng Wang ◽  
Fei Li ◽  
Woliang Yuan
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Matrix Metalloproteinases ◽  
Cardiac Fibroblasts ◽  
Activator Protein 1 ◽  
Activator Protein

Cytokine synergy, collagenases and cartilage collagen breakdown

2003 ◽  
Vol 70 ◽  
pp. 125-133 ◽  
Author(s):  
Tim E. Cawston ◽  
Jenny M. Milner ◽  
Jon B. Catterall ◽  
Andrew D. Rowan
Keyword(s):  
Matrix Metalloproteinases ◽  
Inflammatory Cytokines ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
And Cartilage ◽  
Pro Inflammatory Cytokines

We have investigated proteinases that degrade cartilage collagen. We show that pro-inflammatory cytokines act synergistically with oncastatin M to promote cartilage collagen resorption by the up-regulation and activation of matrix metalloproteinases (MMPs). The precise mechanisms are not known, but involve the up-regulation of c-fos, which binds to MMP promoters at a proximal activator protein-1 (AP-1) site. This markedly up-regulates transcription and leads to higher levels of active MMP proteins.

scholarly journals Long term environmental tobacco smoke activates nuclear transcription factor-kappa B, activator protein-1, and stress responsive kinases in mouse brain

2006 ◽  
Vol 71 (11) ◽  
pp. 1602-1609 ◽  
Author(s):  
Sunil K. Manna ◽  
Thirumalai Rangasamy ◽  
Kimberly Wise ◽  
Shubhashish Sarkar ◽  
Shishir Shishodia ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Mouse Brain ◽  
Environmental Tobacco Smoke ◽  
Tobacco Smoke ◽  
Activator Protein 1 ◽  
Nuclear Transcription Factor ◽  
Activator Protein

Abstract 1380: Antioxidants Decrease Neuronal Angiotensin II Type 1 Receptor in Heart Failure: Inhibition of Activator Protein 1 and Jun N-Terminal Kinase

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Dongmei Liu ◽  
Lie Gao ◽  
Kurtis G Cornish ◽  
Irving H Zucker
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Angiotensin Ii ◽  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Neuronal Cell ◽  
Activator Protein 1 ◽  
Ang Ii ◽  
Nadph Oxidase Activity ◽  
Activator Protein

In a previous study, we showed that Ang II type I receptor (AT1R) expression increased in the rostral ventrolateral medulla (RVLM) of chronic heart failure (CHF) rabbits and in normal rabbits infused with intracerebroventricular (ICV) Angiotensin II (AngII). The present study investigated if oxidative stress plays a role in Ang II induced AT1R upregulation and its relationship to the transcription factor activator protein 1 (AP1) in CHF rabbits and in the CATHa neuronal cell line. In neuronal cell cultures, Ang II significantly increased AT1R mRNA by 153 ± 22%, P <0.01; c-Jun mRNA by 90 ± 10%, P < 0.01; NADPH oxidase activity by 126 ± 43%, P < 0.01 versus untreated cells; Tempol, Apocynin and the AP 1 inhibitor Tanshinone II reversed the increased AT1R, c-Jun expression and NADPH oxidase activity induced by AngII. We examined the effect of ICV Tempol on expression of these proteins in the RVLM of CHF rabbits. Compared to untreated CHF rabbits Tempol significantly decreased AT1R protein expression (0.88±0.16 vs. 1.6±0.29, P <0.05), phosphorylated Jnk protein (0.10±0.02 vs. 0.31±0.10, P <0.05), and phosphorylated c-Jun (0.02±0.001 vs. 0.14±0.05, P <0.05). These data suggest that Ang II induces AT1R upregulation at the transcriptional level by activation of oxidative stress and AP1 in both cultured cells and in intact brain. Antioxidant agents may be beneficial in CHF by decreasing AT1R expression through the Jnk and AP1 pathway.

First molluscan transcription factor activator protein-1 (Ap-1) member from disk abalone and its expression profiling against immune challenge and tissue injury

2010 ◽  
Vol 29 (6) ◽  
pp. 1028-1036 ◽  
Author(s):  
Mahanama De Zoysa ◽  
Chamilani Nikapitiya ◽  
Youngdeuk Lee ◽  
Sukkyoung Lee ◽  
Chulhong Oh ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Expression Profiling ◽  
Tissue Injury ◽  
Activator Protein 1 ◽  
Immune Challenge ◽  
Activator Protein

Activator protein 1 transcription factor fos-related antigen 1 (fra-1) is dispensable for murine liver fibrosis, but modulates xenobiotic metabolism

Hepatology ◽  
2013 ◽  
Vol 59 (1) ◽  
pp. 261-273 ◽  
Author(s):  
Sebastian C. Hasenfuss ◽  
Latifa Bakiri ◽  
Martin K. Thomsen ◽  
Rainer Hamacher ◽  
Erwin F. Wagner
Keyword(s):  
Transcription Factor ◽  
Liver Fibrosis ◽  
Xenobiotic Metabolism ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
Murine Liver
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