scholarly journals p38 mitogen-activated protein kinase/activator protein-1 involved in serum deprivation-induced human alkaline ceramidase 2 upregulation

2014 ◽  
Vol 3 (2) ◽  
pp. 225-229 ◽  
Author(s):  
ZHAOQUAN HUANG ◽  
GUOJIN HUANG ◽  
QUANZHONG LI ◽  
JUNFEI JIN
Keyword(s):  
Protein Kinase ◽  
Serum Deprivation ◽  
Mitogen Activated Protein Kinase ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
Mitogen Activated Protein

scholarly journals Porphyromonas gingivalis Induces Receptor Activator of NF-κB Ligand Expression in Osteoblasts through the Activator Protein 1 Pathway

2004 ◽  
Vol 72 (3) ◽  
pp. 1706-1714 ◽  
Author(s):  
Nobuo Okahashi ◽  
Hiroaki Inaba ◽  
Ichiro Nakagawa ◽  
Taihei Yamamura ◽  
Masae Kuboniwa ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Porphyromonas Gingivalis ◽  
Bone Destruction ◽  
Cysteine Proteases ◽  
Mitogen Activated Protein Kinase ◽  
Activator Protein 1 ◽  
Rankl Expression ◽  
Activator Protein ◽  
Receptor Activator ◽  
Mitogen Activated Protein

ABSTRACT Porphyromonas gingivalis, an important periodontal pathogen, is closely associated with inflammatory alveolar bone resorption, and several components of the organism such as lipopolysaccharides have been reported to stimulate production of cytokines that promote inflammatory bone destruction. We investigated the effect of infection with viable P. gingivalis on cytokine production by osteoblasts. Reverse transcription-PCR and real-time PCR analyses revealed that infection with P. gingivalis induced receptor activator of nuclear factor κB (NF-κB) ligand (RANKL) mRNA expression in mouse primary osteoblasts. Production of interleukin-6 was also stimulated; however, osteoprotegerin was not. SB20350 (an inhibitor of p38 mitogen-activated protein kinase), PD98059 (an inhibitor of classic mitogen-activated protein kinase kinase, MEK1/2), wortmannin (an inhibitor of phosphatidylinositol 3 kinase), and carbobenzoxyl-leucinyl-leucinyl-leucinal (an inhibitor of NF-κB) did not prevent the RANKL expression induced by P. gingivalis. Degradation of inhibitor of NF-κB-alpha was not detectable; however, curcumin, an inhibitor of activator protein 1 (AP-1), prevented the RANKL production induced by P. gingivalis infection. Western blot analysis revealed that phosphorylation of c-Jun, a component of AP-1, occurred in the infected cells, and an analysis of c-Fos binding to an oligonucleotide containing an AP-1 consensus site also demonstrated AP-1 activation in infected osteoblasts. Infection with P. gingivalis KDP136, an isogenic deficient mutant of arginine- and lysine-specific cysteine proteinases, did not stimulate RANKL production. These results suggest that P. gingivalis infection induces RANKL expression in osteoblasts through AP-1 signaling pathways and cysteine proteases of the organism are involved in RANKL production.

scholarly journals Insulin-mediated activation of activator protein-1 through the mitogen-activated protein kinase pathway stimulates collagenase-1 gene transcription in the MES 13 mesangial cell line

2004 ◽  
Vol 33 (1) ◽  
pp. 263-280 ◽  
Author(s):  
JE Ayala ◽  
JN Boustead ◽  
SC Chapman ◽  
CA Svitek ◽  
JK Oeser ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cell Line ◽  
Gene Transcription ◽  
Fusion Gene ◽  
Mitogen Activated Protein Kinase ◽  
Potential Contribution ◽  
Activator Protein 1 ◽  
Promoter Elements ◽  
Activator Protein ◽  
Mitogen Activated Protein

The initial stages of diabetic nephropathy are characterized, in part, by expansion of the mesangial matrix and thickening of the glomerular basement membrane which are caused by increased extracellular matrix (ECM) protein synthesis and reduced degradation, a consequence of decreased matrix metalloproteinase (MMP) activity. These changes have been largely attributed to the effects of hyperglycemia such that the potential contribution of impaired insulin action to alterations in the ECM have not been studied in detail. We have shown here that insulin stimulates collagenase-1 fusion gene transcription in the MES 13 mesangial-derived cell line. Multiple collagenase-1 promoter elements are required for the full stimulatory effect of insulin but the action of insulin appears to be mediated through an activator protein-1 (AP-1) motif. Thus, mutation of this AP-1 motif abolishes insulin-stimulated collagenase fusion gene transcription and, in isolation, this AP-1 motif can mediate a stimulatory effect of insulin on the expression of a heterologous fusion gene. This suggested that the other collagenase-1 promoter elements that are required for the full stimulatory effect of insulin probably bind accessory factors that enhance the effect of insulin mediated through the AP-1 motif. In MES 13 cells, the AP-1 motif is bound by Fra-1, Fra-2, Jun B and Jun D. Stimulation of collagenase-1 fusion gene transcription by insulin requires activation of the mitogen-activated protein kinase (MEK) pathway since inhibition of MEK-1 and -2 blocks this effect. The potential significance of these observations with respect to a role for insulin in the pathophysiology of diabetic glomerulosclerosis is discussed.

Mitogen-activated protein kinase and activator protein-1 dependent signals are essential forBacteroides fragilis enterotoxin-induced enteritis

2005 ◽  
Vol 35 (9) ◽  
pp. 2648-2657 ◽  
Author(s):  
Jung Mogg Kim ◽  
Hwoon Yong Jung ◽  
Jin Young Lee ◽  
Jeehee Youn ◽  
Chul-Hoon Lee ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Mitogen Activated Protein Kinase ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
Mitogen Activated Protein

scholarly journals Cellular signaling by endothelin peptides: pathways to the nucleus.

1992 ◽  
Vol 2 (10) ◽  
pp. S116
Author(s):  
M S Simonson ◽  
Y Wang ◽  
M J Dunn
Keyword(s):  
Protein Kinase ◽  
Mesangial Cells ◽  
Regulatory Peptides ◽  
Mitogen Activated Protein Kinase ◽  
Activator Protein 1 ◽  
Glomerular Mesangial Cells ◽  
Short Term ◽  
Activator Protein ◽  
Mitogen Activated Protein

Endothelins (ET) are potent regulatory peptides that evoke diverse responses in glomerular mesangial cells. These include short-term actions, such as contraction and secretion, and long-term, adaptive responses, such as cell growth. Although much attention has been focused on the second messenger cascades, which govern short-term effects, the pathways of cytosolic and nuclear signaling, which effect long-term changes, remain unclear. Several distal signaling events by ET receptors have been characterized in rat mesangial cells. These include activation of a cytosolic protein kinase, mitogen-activated protein kinase and an inducible transcription factor, activator protein-1 (AP-1). This review focuses on the activation of mitogen-activated protein kinase and activator protein-1 by ET and discusses the potential role of these third and fourth messengers in controlling long-term cellular adaptations. Characterization of these and other cytosolic and nuclear signals should provide important insights into the pleiotropic actions of ET peptides.

The mitogen-activated protein kinase p38 regulates activator protein 1 by direct phosphorylation of c-Jun

2007 ◽  
Vol 39 (12) ◽  
pp. 2278-2288 ◽  
Author(s):  
Matjaz Humar ◽  
Torsten Loop ◽  
Rene Schmidt ◽  
Alexander Hoetzel ◽  
Martin Roesslein ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Mitogen Activated Protein Kinase ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
Mitogen Activated Protein
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