Tumor Necrosis Factor-{alpha} Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor- -activated Kinase 1 (TAK1)-dependent Signaling Pathway.

Tumor Necrosis Factor-{alpha} Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor- -activated Kinase 1 (TAK1)-dependent Signaling Pathway. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Tumor Necrosis Factor-{alpha} Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor- -activated Kinase 1 (TAK1)-dependent Signaling Pathway. Abstract Text:

Apurva K Srivastava,Xuezhong Qin,Nia Wedhas,Marc Arnush,Thomas A Linkhart,Robert B Chadwick,Ashok Kumar,Apurva K Srivastava,Xuezhong Qin,Nia Wedhas,Marc Arnush,Thomas A Linkhart,Robert B Chadwick,Ashok Kumar,Apurva K Srivastava,Xuezhong Qin,Nia Wedhas,Marc Arnush,Thomas A Linkhart,Robert B Chadwick,Ashok Kumar,

We have investigated the effect of tumor necrosis factor-alpha (TNF-alpha) on the production of extracellular matrix-degrading proteases in skeletal muscles. Using microarray, quantitative PCR, Western blotting, and zymography, we found that TNF-alpha drastically increases the production of matrix metalloproteinase (MMP)-9 from C2C12 myotubes. In vivo administration of TNF-alpha in mice increased the transcript level of MMP-9 in skeletal muscle tissues. Although TNF-alpha activated all the three MAPKs (i.e. ERK1/2, JNK, and p38), inhibition of ERK1/2 or p38 but not JNK blunted the TNF-alpha-induced production of MMP-9 from myotubes. Inhibition of Akt also inhibited the TNF-alpha-induced production of MMP-9. TNF-alpha increased the activation of transcription factors NF-kappaB and AP-1 but not SP-1 in myotubes. Overexpression of a dominant negative inhibitor of NF-kappaB or AP-1 blocked the TNF-alpha-induced expression of MMP-9 in myotubes. Similarly, point mutations in AP-1- or NF-kappaB-binding sites in MMP-9 promoter inhibited the TNF-alpha-induced expression of a reporter gene. TNF-alpha increased the activity of transforming growth factor-beta-activating kinase-1 (TAK1). Furthermore, overexpression of a dominant negative mutant of TAK1 blocked the TNF-alpha-induced expression of MMP-9 and activation of NF-kappaB and AP-1. Our results also suggest that TNF-alpha induces MMP-9 expression in muscle cells through the recruitment of TRAF-2, Fas-associated protein with death domain, and TNF receptor-associated protein with death domain but not NIK or TRAF-6 proteins. We conclude that TAK1-mediated pathways are involved in TNF-alpha-induced MMP-9 production in skeletal muscle cells.

Tumor Necrosis Factor-{alpha} Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor- -activated Kinase 1 (TAK1)-dependent Signaling Pathway. Publishing Authors By Initials

AK Srivastava,X Qin,N Wedhas,M Arnush,TA Linkhart,RB Chadwick,A Kumar,AK Srivastava,X Qin,N Wedhas,M Arnush,TA Linkhart,RB Chadwick,A Kumar,AK Srivastava,X Qin,N Wedhas,M Arnush,TA Linkhart,RB Chadwick,A Kumar,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Tumor Necrosis Factor-{alpha} Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor- -activated Kinase 1 (TAK1)-dependent Signaling Pathway. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: The Journal of biological chemistry

VOLUME: 282

Page Numbers: 35113-24

Journal Abbreviation: J. Biol. Chem.

ISSN: 0021-9258

DAY: 26

MONTH: 09

YEAR: 2007

Tumor Necrosis Factor-{alpha} Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor- -activated Kinase 1 (TAK1)-dependent Signaling Pathway. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985121

Tumor Necrosis Factor-{alpha} Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor- -activated Kinase 1 (TAK1)-dependent Signaling Pathway. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Tumor Necrosis Factor-{alpha} Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor- -activated Kinase 1 (TAK1)-dependent Signaling Pathway. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Tumor Necrosis Factor-{alpha} Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor- -activated Kinase 1 (TAK1)-dependent Signaling Pathway.

AFFILIATION: Jerry L. Pettis Memorial Veterans Affairs Medical Center, Loma Linda, California 92357.

Country: United States

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: J Biol Chem

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Tumor Necrosis Factor-{alpha} Augments Matrix Metalloproteinase-9 Production in Skeletal Muscle Cells through the Activation of Transforming Growth Factor- -activated Kinase 1 TAK1-dependent Signaling Pathway Related Publications

• A modified Plasmodium falciparum growth inhibition assay (GIA) to assess activity of plasma from malaria endemic areas.
• A new paradigm for the treatment of high-risk prostate cancer: radiosensitization with docetaxel.
• An inherent role of microtubule network in the action of nuclear receptor.
• Antibody responses to Plasmodium falciparum vaccine candidate antigens in three areas distinct with respect to altitude.
• Breast cancer-amplified sequence 3, a target of metastasis-associated protein 1, contributes to tamoxifen resistance in premenopausal patients with breast cancer.
• Ciz1, a Novel DNA-binding coactivator of the estrogen receptor alpha, confers hypersensitivity to estrogen action.
• Cognitive function in adults with type 2 diabetes and major depression.
• Diagnosis and management of extensive vertex birth molding.
• Dynein light chain 1, a p21-activated kinase 1-interacting substrate, promotes cancerous phenotypes.
• Effect of individual and multiple antioxidant vitamins on growth and morphology of human nontumorigenic and tumorigenic parotid acinar cells in culture.
• Functional analysis of alternative isoforms of the transcription factor PAX3 in melanocytes in vitro.
• HPA axis activity and neuropathogenesis in HIV-1 clade C infection.
• How substance use differs among American secondary schools.
• Influence of Agrobacterium rhizogenes Strains on Biomass and Alkaloid Productivity in Hairy Root Lines of Hyoscyamus muticus and H. albus *.
• Letter to the editor: The suckling-micturition reflex in cows.
• Metal-binding properties of human centrin-2 determined by micro-electrospray ionization mass spectrometry and UV spectroscopy.
• Metastasis tumor antigens, an emerging family of multifaceted master coregulators.
• Metastatic tumor antigen 3 is a direct corepressor of the Wnt4 pathway.
• Modification of the expression of adenosine 3',5'-cyclic monophosphate-induced differentiated functions in neuroblastoma cells by beta-carotene and D-alpha-tocopheryl succinate.
• P21-activated kinases in human cancer.
• Pituitary abscess: Report of four cases and review of literature.
• Potential medicinal plants for CNS disorders: an overview.
• Protein disulfide isomerase assisted protein folding in malaria parasites.
• Quality of life in HIV subtype C infection among asymptomatic subjects and its association with CD4 counts and viral loads--a study from South India.
• Re-engineering cytochrome P450 2B11dH for enhanced metabolism of several substrates including the anti-cancer prodrugs cyclophosphamide and ifosfamide.
• Sexual differentiation and development in the malaria parasite.
• Standard wound coverage techniques for extremity war injury.
• Systemic, cellular and molecular analysis of chemoreflex-mediated sympathoexcitation by chronic intermittent hypoxia.
• Variable region 4 of SIV envelope correlates with rapid disease progression in morphine-exposed macaques infected with SIV/SHIV.
• p21-activated kinase signaling in breast cancer.