Stimulation of FasL Induces Production of Proinflammatory Mediators Through Activation of Mitogen-Activated Protein Kinases and Nuclear Factor-κB in THP-1 Cells

Inflammation ◽  
2010 ◽  
Vol 35 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Sang-Min Lee ◽  
Eun-Ju Kim ◽  
Kyoungho Suk ◽  
Won-Ha Lee
Keyword(s):  
Protein Kinases ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Mitogen Activated Protein Kinases ◽  
Proinflammatory Mediators ◽  
Mitogen Activated Protein ◽  
Stimulation Of

scholarly journals Bacteroides fragilis Enterotoxin Induces Intestinal Epithelial Cell Secretion of Interleukin-8 through Mitogen-Activated Protein Kinases and a Tyrosine Kinase-Regulated Nuclear Factor-κB Pathway

2004 ◽  
Vol 72 (10) ◽  
pp. 5832-5839 ◽  
Author(s):  
Shaoguang Wu ◽  
Jan Powell ◽  
Nes Mathioudakis ◽  
Sheryl Kane ◽  
Ellen Fernandez ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Protein Kinases ◽  
Bacteroides Fragilis ◽  
Nuclear Factor Κb ◽  
Interleukin 8 ◽  
Biologically Active ◽  
Nuclear Factor ◽  
Intestinal Epithelial ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein

ABSTRACT Enterotoxigenic Bacteroides fragilis (ETBF) secretes a 20-kDa metalloprotease toxin termed B. fragilis toxin (BFT). ETBF disease in animals is associated with an acute inflammatory response in the intestinal mucosa, and lethal hemorrhagic colitis may occur in rabbits. In this study, we confirmed recent reports (J. M. Kim, Y. K. Oh, Y. J. Kim, H. B. Oh, and Y. J. Cho, Clin. Exp. Immunol. 123:421-427, 2001; L. Sanfilippo, C. K. Li, R. Seth, T. J. Balwin, M. J. Menozzi, and Y. R. Mahida, Clin. Exp. Immunol. 119:456-463, 2000) that purified BFT stimulates interleukin-8 (IL-8) secretion by human intestinal epithelial cells (HT29/C1 cells) and demonstrate that stimulation of IL-8 production is dependent on biologically active BFT and independent of serum. Induction of IL-8 mRNA expression occurs rapidly and ceases by 6 h after BFT treatment, whereas IL-8 secretion continues to increase for at least 18 h. Our data suggest that BFT-stimulated IL-8 secretion involves tyrosine kinase-dependent activation of nuclear factor-κB (NF-κB) as well as activation of the mitogen-activated protein kinases (MAPKs), p38 and extracellular signal-related kinase. Simultaneous activation of NF-κB and MAPKs appears necessary for secretion of IL-8 by HT29/C1 cells treated with BFT.

scholarly journals Interaction Among Mitochondria, Mitogen-Activated Protein Kinases, and Nuclear Factor-κB in Cellular Models of Parkinson's Disease

2002 ◽  
Vol 74 (4) ◽  
pp. 1384-1392 ◽  
Author(s):  
David S. Cassarino ◽  
Erik M. Halvorsen ◽  
Russell H. Swerdlow ◽  
Nicole N. Abramova ◽  
W. Davis Parker ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protein Kinases ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Mitogen Activated Protein Kinases ◽  
Cellular Models ◽  
Mitogen Activated Protein

Knockdown of lncRNA LINC00707 alleviates LPS-induced injury in MRC-5 cells by acting as a ceRNA of miR-223-5p

2021 ◽  
Vol 85 (2) ◽  
pp. 315-323
Author(s):  
Xiequn Zou ◽  
Cheng Gao ◽  
Rong Shang ◽  
Huan Chen ◽  
Bing Wang
Keyword(s):  
Cell Viability ◽  
Protein Kinases ◽  
Respiratory Disease ◽  
Noncoding Rnas ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein ◽  
Apoptosis And Inflammation ◽  
Therapeutic Avenue

ABSTRACT Pneumonia is a common respiratory disease worldwide. Long noncoding RNAs have been implicated in the pathogenesis of pneumonia. However, the effect and mechanism of long intergenic nonprotein-coding RNA (LINC00707) on pneumonia pathogenesis were still unclear. Lipopolysaccharide (LPS) reduced cell viability and promoted apoptosis and inflammation in MRC-5 cells. LINC00707 was increased, and miR-223-5p was decreased in LPS-treated MRC-5 cells. LINC00707 knockdown relieved LPS-triggered injury in MRC-5 cells. LINC00707 directly interacted with miR-223-5p through acting as a miR-223-5p sponge. Moreover, miR-223-5p mediated the regulation of LINC00707 silencing on LPS-stimulated cytotoxicity in MRC-5 cells. p38 mitogen-activated protein kinases and nuclear factor-κB signaling pathways were modulated by the LINC00707/miR-223-5p axis in LPS-induced MRC-5 cells. Our present study indicated that LINC00707 depletion alleviated LPS-induced injury in MRC-5 cells at least partly by acting as a sponge of miR-223-5p, highlighting a new potential therapeutic avenue for pneumonia treatment.

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