Campylobacter jejuni activates mitogen-activated protein kinases in Caco-2 cell monolayers and in vitro infected primary human colonic tissue

Microbiology ◽  
2005 ◽  
Vol 151 (8) ◽  
pp. 2765-2772 ◽  
Author(s):  
Amanda MacCallum ◽  
Graham Haddock ◽  
Paul H. Everest
Keyword(s):  
Protein Kinases ◽  
Campylobacter Jejuni ◽  
Inflammatory Responses ◽  
Host Responses ◽  
Epithelial Cell Line ◽  
Colonic Tissue ◽  
Mitogen Activated Protein Kinases ◽  
Cell Monolayers ◽  
Mitogen Activated Protein

The mitogen-activated protein kinases (MAPKs) play a central role in many host signalling pathways. These signalling proteins are known to be involved in host responses against invasive bacteria including generation of chemotactic and inflammatory cytokines. It was hypothesized that Campylobacter jejuni may activate MAPKs, as intestinal infection may induce a clinical and pathological picture of acute colonic inflammation. Infection of Caco-2 cell monolayers (human colonic epithelial cell line) and human colonic tissue with C. jejuni in vitro demonstrated increased MAPK activity for ERK 1/2 (p44/42 MAPK), JNK and p38 MAPKs. Kinase activity and phosphorylated forms were increased in infected Caco-2 cells and human colonic explants, suggesting that these pathways are important in inflammatory responses induced by C. jejuni in man.

scholarly journals Expression and activity of mitogen activated protein kinases in human colorectal carcinoma

Gut ◽  
1999 ◽  
Vol 44 (6) ◽  
pp. 834-838 ◽  
Author(s):  
S Eggstein ◽  
M Franke ◽  
I Kutschka ◽  
G Manthey ◽  
B U von Specht ◽  
...  
Keyword(s):  
Protein Kinases ◽  
Normal Mucosa ◽  
Mitogen Activated Protein Kinases ◽  
Colorectal Mucosa ◽  
Mapk Activity ◽  
Mitogen Activated Protein ◽  
Colonic Carcinogenesis ◽  
Cell Growth And Differentiation ◽  
Expression And Activity

BACKGROUNDMitogen activated protein kinases (MAPKs) play a central role in the regulation of both cell growth and differentiation. They are involved in signal transduction of oncogenes and growth factors. The role of MAPK in colonic carcinoma is unknown.AIMSTo establish whether the expression and activity of p42/44 MAPKs are altered in colorectal tumours as compared with normal mucosa.METHODSThe expression and activity of p42/p44 MAPK were investigated in 22 colorectal carcinomas, four adenomas, and the corresponding normal colorectal mucosa by the use of western blotting, immunoprecipitation, and in vitro kinase assays.RESULTSAfter immunoprecipitation with an antibody specific for p42 MAPK, we found significant inactivation of p42 MAPK in colonic carcinomas as well as in adenomas, whereas most sample pairs showed only minor differences in p42 MAPK expression. Investigation of MAPK with an antibody capable of detecting both p42 and p44 MAPK showed a slight but significant decrease in p44 MAPK content in malignant tissues. With this antibody, only minor alterations in MAPK activity and no correlation with p42 MAPK activity were found.CONCLUSIONSInactivation of p42 MAPK could be associated with colonic carcinogenesis.

scholarly journals Activation of mitogen-activated protein kinases by a splice variant of GHRH receptor

2009 ◽  
Vol 44 (2) ◽  
pp. 127-134 ◽  
Author(s):  
Nektarios Barabutis ◽  
Agnieszka Siejka ◽  
Andrew V Schally ◽  
Norman L Block ◽  
Renzhi Cai ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Protein Kinases ◽  
Mechanism Of Action ◽  
Intracellular Signaling ◽  
Splice Variants ◽  
Nuclear Antigen ◽  
Proliferative Cell Nuclear Antigen ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein

Hypothalamic GHRH controls the release of GH from the pituitary gland and also acts as a growth factor in a variety of cancers. The mitogenetic activity of GHRH is exerted through the binding to the pituitary type receptor (pGHRH-R) and its splice variants, mainly SV1. The intracellular signaling pathways that are activated upon the binding of GHRH to the SV1 receptor have not been elucidated. HeLa cervical cancer cells do not express GHRH or GHRH receptors (GHRHRs) and thus do not respond to GHRH or GHRH antagonists. In order to elucidate the mechanism of action of SV1 receptor, we transfected HeLa cells with plasmids for pcDNA3-GHRHR or pcDNA3-SV1. The transfected cells responded to both GHRH (1–29)NH2 and GHRH antagonist MZ-5-156, as shown by an increase or decrease respectively in the proliferation rate in vitro and the expression of proliferative cell nuclear antigen. We also demonstrated that when the cells transfected with SV1 plasmid are stimulated with GHRH (1–29)NH2, SV1 receptor activates the mitogen-activated protein kinases pathway (MAPKs), as shown previously for the cells that express pGHRH-R. Our results show, for the first time, the activation of the MAPKs cascade by the SV1 receptor. Since SV1 receptor is found in various tumors and mediates the responses to GHRH and synthetic antagonists, our findings shed light on the mechanism of action of SV1 receptor in cancer cells.

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