Cyclic AMP Inhibition of Tumor Necrosis Factor α Production Induced by Amyloidogenic C-Terminal Peptide of Alzheimer's Amyloid Precursor Protein in Macrophages: Involvement of Multiple Intracellular Pathways and Cyclic AMP Response Element Binding Protein

2003 ◽  
Vol 63 (3) ◽  
pp. 690-698 ◽  
Author(s):  
Young Hae Chong ◽  
Yoo Jung Shin ◽  
Yoo-Hun Suh
Keyword(s):  
Tumor Necrosis Factor ◽  
Cyclic Amp ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Element Binding Protein ◽  
Cyclic Amp Response Element ◽  
Intracellular Pathways ◽  
Factor Α ◽  
Amp Inhibition ◽  
Necrosis Factor

Release of Tumor Necrosis Factor-α from Coronary Smooth Muscle: Activation of NF-κB and Inhibition by Elevated Cyclic AMP

1998 ◽  
Vol 80 (2) ◽  
pp. 129-135 ◽  
Author(s):  
Walter H. Newman ◽  
Li-Ming Zhang ◽  
Dong H. Lee ◽  
Martin L. Dalton ◽  
Debra J. Warejcka ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Tumor Necrosis Factor ◽  
Cyclic Amp ◽  
Tumor Necrosis ◽  
Muscle Activation ◽  
Tumor Necrosis Factor Α ◽  
Coronary Smooth Muscle ◽  
Factor Α ◽  
Necrosis Factor

Cyclic AMP and tumor necrosis factor-α regulate CXCR4 gene expression in Schwann cells

2003 ◽  
Vol 24 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Patrick Küry ◽  
Hubertus Köller ◽  
Michael Hamacher ◽  
Christiane Cornely ◽  
Birgit Hasse ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumor Necrosis Factor ◽  
Cyclic Amp ◽  
Schwann Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Differential Activation of the Transcription Factor Cyclic AMP Response Element Binding Protein (CREB) in Macrophages following Infection with Pathogenic and Nonpathogenic Mycobacteria and Role for CREB in Tumor Necrosis Factor Alpha Production

2005 ◽  
Vol 73 (1) ◽  
pp. 514-522 ◽  
Author(s):  
Shannon K. Roach ◽  
Seong-Beom Lee ◽  
Jeffrey S. Schorey
Keyword(s):  
Transcription Factor ◽  
Tumor Necrosis Factor ◽  
Cyclic Amp ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Element Binding Protein ◽  
Cyclic Amp Response Element ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Previous studies in our laboratory have shown a differential activation of the mitogen-activated protein kinases (MAPKs) in primary bone marrow-derived macrophages following infection with pathogenic Mycobacterium avium compared to the activation following infection with nonpathogenic Mycobacterium smegmatis. Additionally, M. smegmatis-infected macrophages produced significantly elevated levels of tumor necrosis factor alpha (TNF-α) compared to the levels produced by M. avium-infected macrophages. The TNF-α production was dependent on both p38 and extracellular signal-regulated kinase 1/2 (ERK 1/2) activation. However, the macrophage transcription factors downstream of the MAPKs, which were required for TNF-α production, remained undefined. In this study we determined that the transcription factor cyclic AMP response element binding protein (CREB) is significantly more activated in M. smegmatis-infected macrophages than in M. avium-infected macrophages. We also found that CREB activation was dependent on p38 and protein kinase A but not on ERK 1/2 or calmodulin kinase II. Moreover, mutating the cAMP-responsive element on the TNF-α promoter resulted in significantly diminished promoter activity following M. smegmatis infection but not M. avium infection. The inability of macrophages infected with M. avium to sustain MAPK activation and to produce high levels of TNF-α was due, in part, to an increase in serine/threonine phosphatase PP2A activity. Our studies are the first to demonstrate an important role for the transcription factor CREB in TNF-α production by mycobacterium-infected macrophages, as well as a role for M. avium's induction of PP2A phosphatase activity as a mechanism to limit macrophage activation.

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